Pleiotropic Actions of Aldehyde Reductase (AKR1A)
We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via t...
Ausführliche Beschreibung
Autor*in: |
Junichi Fujii [verfasserIn] Takujiro Homma [verfasserIn] Satoshi Miyata [verfasserIn] Motoko Takahashi [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2021 |
---|
Schlagwörter: |
---|
Übergeordnetes Werk: |
In: Metabolites - MDPI AG, 2012, 11(2021), 6, p 343 |
---|---|
Übergeordnetes Werk: |
volume:11 ; year:2021 ; number:6, p 343 |
Links: |
---|
DOI / URN: |
10.3390/metabo11060343 |
---|
Katalog-ID: |
DOAJ016784510 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | DOAJ016784510 | ||
003 | DE-627 | ||
005 | 20240412180143.0 | ||
007 | cr uuu---uuuuu | ||
008 | 230226s2021 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.3390/metabo11060343 |2 doi | |
035 | |a (DE-627)DOAJ016784510 | ||
035 | |a (DE-599)DOAJ9db845b68e3547c69aa8797874e244f4 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
050 | 0 | |a QR1-502 | |
100 | 0 | |a Junichi Fujii |e verfasserin |4 aut | |
245 | 1 | 0 | |a Pleiotropic Actions of Aldehyde Reductase (AKR1A) |
264 | 1 | |c 2021 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a Computermedien |b c |2 rdamedia | ||
338 | |a Online-Ressource |b cr |2 rdacarrier | ||
520 | |a We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. | ||
650 | 4 | |a <i<Akr1a</i< | |
650 | 4 | |a <i<Akr1b</i< | |
650 | 4 | |a reductive detoxification | |
650 | 4 | |a glycation | |
650 | 4 | |a ascorbate synthesis | |
650 | 4 | |a S-nitrosylation | |
653 | 0 | |a Microbiology | |
700 | 0 | |a Takujiro Homma |e verfasserin |4 aut | |
700 | 0 | |a Satoshi Miyata |e verfasserin |4 aut | |
700 | 0 | |a Motoko Takahashi |e verfasserin |4 aut | |
773 | 0 | 8 | |i In |t Metabolites |d MDPI AG, 2012 |g 11(2021), 6, p 343 |w (DE-627)718627164 |w (DE-600)2662251-8 |x 22181989 |7 nnns |
773 | 1 | 8 | |g volume:11 |g year:2021 |g number:6, p 343 |
856 | 4 | 0 | |u https://doi.org/10.3390/metabo11060343 |z kostenfrei |
856 | 4 | 0 | |u https://doaj.org/article/9db845b68e3547c69aa8797874e244f4 |z kostenfrei |
856 | 4 | 0 | |u https://www.mdpi.com/2218-1989/11/6/343 |z kostenfrei |
856 | 4 | 2 | |u https://doaj.org/toc/2218-1989 |y Journal toc |z kostenfrei |
912 | |a GBV_USEFLAG_A | ||
912 | |a SYSFLAG_A | ||
912 | |a GBV_DOAJ | ||
912 | |a GBV_ILN_20 | ||
912 | |a GBV_ILN_22 | ||
912 | |a GBV_ILN_23 | ||
912 | |a GBV_ILN_24 | ||
912 | |a GBV_ILN_39 | ||
912 | |a GBV_ILN_40 | ||
912 | |a GBV_ILN_60 | ||
912 | |a GBV_ILN_62 | ||
912 | |a GBV_ILN_63 | ||
912 | |a GBV_ILN_65 | ||
912 | |a GBV_ILN_69 | ||
912 | |a GBV_ILN_70 | ||
912 | |a GBV_ILN_73 | ||
912 | |a GBV_ILN_74 | ||
912 | |a GBV_ILN_95 | ||
912 | |a GBV_ILN_105 | ||
912 | |a GBV_ILN_110 | ||
912 | |a GBV_ILN_151 | ||
912 | |a GBV_ILN_161 | ||
912 | |a GBV_ILN_170 | ||
912 | |a GBV_ILN_213 | ||
912 | |a GBV_ILN_230 | ||
912 | |a GBV_ILN_285 | ||
912 | |a GBV_ILN_293 | ||
912 | |a GBV_ILN_602 | ||
912 | |a GBV_ILN_2014 | ||
912 | |a GBV_ILN_4012 | ||
912 | |a GBV_ILN_4037 | ||
912 | |a GBV_ILN_4112 | ||
912 | |a GBV_ILN_4125 | ||
912 | |a GBV_ILN_4126 | ||
912 | |a GBV_ILN_4249 | ||
912 | |a GBV_ILN_4305 | ||
912 | |a GBV_ILN_4306 | ||
912 | |a GBV_ILN_4307 | ||
912 | |a GBV_ILN_4313 | ||
912 | |a GBV_ILN_4322 | ||
912 | |a GBV_ILN_4323 | ||
912 | |a GBV_ILN_4324 | ||
912 | |a GBV_ILN_4325 | ||
912 | |a GBV_ILN_4338 | ||
912 | |a GBV_ILN_4367 | ||
912 | |a GBV_ILN_4700 | ||
951 | |a AR | ||
952 | |d 11 |j 2021 |e 6, p 343 |
author_variant |
j f jf t h th s m sm m t mt |
---|---|
matchkey_str |
article:22181989:2021----::litoiatosfleyee |
hierarchy_sort_str |
2021 |
callnumber-subject-code |
QR |
publishDate |
2021 |
allfields |
10.3390/metabo11060343 doi (DE-627)DOAJ016784510 (DE-599)DOAJ9db845b68e3547c69aa8797874e244f4 DE-627 ger DE-627 rakwb eng QR1-502 Junichi Fujii verfasserin aut Pleiotropic Actions of Aldehyde Reductase (AKR1A) 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. <i<Akr1a</i< <i<Akr1b</i< reductive detoxification glycation ascorbate synthesis S-nitrosylation Microbiology Takujiro Homma verfasserin aut Satoshi Miyata verfasserin aut Motoko Takahashi verfasserin aut In Metabolites MDPI AG, 2012 11(2021), 6, p 343 (DE-627)718627164 (DE-600)2662251-8 22181989 nnns volume:11 year:2021 number:6, p 343 https://doi.org/10.3390/metabo11060343 kostenfrei https://doaj.org/article/9db845b68e3547c69aa8797874e244f4 kostenfrei https://www.mdpi.com/2218-1989/11/6/343 kostenfrei https://doaj.org/toc/2218-1989 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 6, p 343 |
spelling |
10.3390/metabo11060343 doi (DE-627)DOAJ016784510 (DE-599)DOAJ9db845b68e3547c69aa8797874e244f4 DE-627 ger DE-627 rakwb eng QR1-502 Junichi Fujii verfasserin aut Pleiotropic Actions of Aldehyde Reductase (AKR1A) 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. <i<Akr1a</i< <i<Akr1b</i< reductive detoxification glycation ascorbate synthesis S-nitrosylation Microbiology Takujiro Homma verfasserin aut Satoshi Miyata verfasserin aut Motoko Takahashi verfasserin aut In Metabolites MDPI AG, 2012 11(2021), 6, p 343 (DE-627)718627164 (DE-600)2662251-8 22181989 nnns volume:11 year:2021 number:6, p 343 https://doi.org/10.3390/metabo11060343 kostenfrei https://doaj.org/article/9db845b68e3547c69aa8797874e244f4 kostenfrei https://www.mdpi.com/2218-1989/11/6/343 kostenfrei https://doaj.org/toc/2218-1989 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 6, p 343 |
allfields_unstemmed |
10.3390/metabo11060343 doi (DE-627)DOAJ016784510 (DE-599)DOAJ9db845b68e3547c69aa8797874e244f4 DE-627 ger DE-627 rakwb eng QR1-502 Junichi Fujii verfasserin aut Pleiotropic Actions of Aldehyde Reductase (AKR1A) 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. <i<Akr1a</i< <i<Akr1b</i< reductive detoxification glycation ascorbate synthesis S-nitrosylation Microbiology Takujiro Homma verfasserin aut Satoshi Miyata verfasserin aut Motoko Takahashi verfasserin aut In Metabolites MDPI AG, 2012 11(2021), 6, p 343 (DE-627)718627164 (DE-600)2662251-8 22181989 nnns volume:11 year:2021 number:6, p 343 https://doi.org/10.3390/metabo11060343 kostenfrei https://doaj.org/article/9db845b68e3547c69aa8797874e244f4 kostenfrei https://www.mdpi.com/2218-1989/11/6/343 kostenfrei https://doaj.org/toc/2218-1989 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 6, p 343 |
allfieldsGer |
10.3390/metabo11060343 doi (DE-627)DOAJ016784510 (DE-599)DOAJ9db845b68e3547c69aa8797874e244f4 DE-627 ger DE-627 rakwb eng QR1-502 Junichi Fujii verfasserin aut Pleiotropic Actions of Aldehyde Reductase (AKR1A) 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. <i<Akr1a</i< <i<Akr1b</i< reductive detoxification glycation ascorbate synthesis S-nitrosylation Microbiology Takujiro Homma verfasserin aut Satoshi Miyata verfasserin aut Motoko Takahashi verfasserin aut In Metabolites MDPI AG, 2012 11(2021), 6, p 343 (DE-627)718627164 (DE-600)2662251-8 22181989 nnns volume:11 year:2021 number:6, p 343 https://doi.org/10.3390/metabo11060343 kostenfrei https://doaj.org/article/9db845b68e3547c69aa8797874e244f4 kostenfrei https://www.mdpi.com/2218-1989/11/6/343 kostenfrei https://doaj.org/toc/2218-1989 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 6, p 343 |
allfieldsSound |
10.3390/metabo11060343 doi (DE-627)DOAJ016784510 (DE-599)DOAJ9db845b68e3547c69aa8797874e244f4 DE-627 ger DE-627 rakwb eng QR1-502 Junichi Fujii verfasserin aut Pleiotropic Actions of Aldehyde Reductase (AKR1A) 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. <i<Akr1a</i< <i<Akr1b</i< reductive detoxification glycation ascorbate synthesis S-nitrosylation Microbiology Takujiro Homma verfasserin aut Satoshi Miyata verfasserin aut Motoko Takahashi verfasserin aut In Metabolites MDPI AG, 2012 11(2021), 6, p 343 (DE-627)718627164 (DE-600)2662251-8 22181989 nnns volume:11 year:2021 number:6, p 343 https://doi.org/10.3390/metabo11060343 kostenfrei https://doaj.org/article/9db845b68e3547c69aa8797874e244f4 kostenfrei https://www.mdpi.com/2218-1989/11/6/343 kostenfrei https://doaj.org/toc/2218-1989 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021 6, p 343 |
language |
English |
source |
In Metabolites 11(2021), 6, p 343 volume:11 year:2021 number:6, p 343 |
sourceStr |
In Metabolites 11(2021), 6, p 343 volume:11 year:2021 number:6, p 343 |
format_phy_str_mv |
Article |
institution |
findex.gbv.de |
topic_facet |
<i<Akr1a</i< <i<Akr1b</i< reductive detoxification glycation ascorbate synthesis S-nitrosylation Microbiology |
isfreeaccess_bool |
true |
container_title |
Metabolites |
authorswithroles_txt_mv |
Junichi Fujii @@aut@@ Takujiro Homma @@aut@@ Satoshi Miyata @@aut@@ Motoko Takahashi @@aut@@ |
publishDateDaySort_date |
2021-01-01T00:00:00Z |
hierarchy_top_id |
718627164 |
id |
DOAJ016784510 |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ016784510</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240412180143.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2021 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3390/metabo11060343</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ016784510</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ9db845b68e3547c69aa8797874e244f4</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QR1-502</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Junichi Fujii</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Pleiotropic Actions of Aldehyde Reductase (AKR1A)</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<Akr1a</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<Akr1b</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">reductive detoxification</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">glycation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ascorbate synthesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">S-nitrosylation</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Microbiology</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Takujiro Homma</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Satoshi Miyata</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Motoko Takahashi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Metabolites</subfield><subfield code="d">MDPI AG, 2012</subfield><subfield code="g">11(2021), 6, p 343</subfield><subfield code="w">(DE-627)718627164</subfield><subfield code="w">(DE-600)2662251-8</subfield><subfield code="x">22181989</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:11</subfield><subfield code="g">year:2021</subfield><subfield code="g">number:6, p 343</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3390/metabo11060343</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/9db845b68e3547c69aa8797874e244f4</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.mdpi.com/2218-1989/11/6/343</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2218-1989</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">11</subfield><subfield code="j">2021</subfield><subfield code="e">6, p 343</subfield></datafield></record></collection>
|
callnumber-first |
Q - Science |
author |
Junichi Fujii |
spellingShingle |
Junichi Fujii misc QR1-502 misc <i<Akr1a</i< misc <i<Akr1b</i< misc reductive detoxification misc glycation misc ascorbate synthesis misc S-nitrosylation misc Microbiology Pleiotropic Actions of Aldehyde Reductase (AKR1A) |
authorStr |
Junichi Fujii |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)718627164 |
format |
electronic Article |
delete_txt_mv |
keep |
author_role |
aut aut aut aut |
collection |
DOAJ |
remote_str |
true |
callnumber-label |
QR1-502 |
illustrated |
Not Illustrated |
issn |
22181989 |
topic_title |
QR1-502 Pleiotropic Actions of Aldehyde Reductase (AKR1A) <i<Akr1a</i< <i<Akr1b</i< reductive detoxification glycation ascorbate synthesis S-nitrosylation |
topic |
misc QR1-502 misc <i<Akr1a</i< misc <i<Akr1b</i< misc reductive detoxification misc glycation misc ascorbate synthesis misc S-nitrosylation misc Microbiology |
topic_unstemmed |
misc QR1-502 misc <i<Akr1a</i< misc <i<Akr1b</i< misc reductive detoxification misc glycation misc ascorbate synthesis misc S-nitrosylation misc Microbiology |
topic_browse |
misc QR1-502 misc <i<Akr1a</i< misc <i<Akr1b</i< misc reductive detoxification misc glycation misc ascorbate synthesis misc S-nitrosylation misc Microbiology |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
cr |
hierarchy_parent_title |
Metabolites |
hierarchy_parent_id |
718627164 |
hierarchy_top_title |
Metabolites |
isfreeaccess_txt |
true |
familylinks_str_mv |
(DE-627)718627164 (DE-600)2662251-8 |
title |
Pleiotropic Actions of Aldehyde Reductase (AKR1A) |
ctrlnum |
(DE-627)DOAJ016784510 (DE-599)DOAJ9db845b68e3547c69aa8797874e244f4 |
title_full |
Pleiotropic Actions of Aldehyde Reductase (AKR1A) |
author_sort |
Junichi Fujii |
journal |
Metabolites |
journalStr |
Metabolites |
callnumber-first-code |
Q |
lang_code |
eng |
isOA_bool |
true |
recordtype |
marc |
publishDateSort |
2021 |
contenttype_str_mv |
txt |
author_browse |
Junichi Fujii Takujiro Homma Satoshi Miyata Motoko Takahashi |
container_volume |
11 |
class |
QR1-502 |
format_se |
Elektronische Aufsätze |
author-letter |
Junichi Fujii |
doi_str_mv |
10.3390/metabo11060343 |
author2-role |
verfasserin |
title_sort |
pleiotropic actions of aldehyde reductase (akr1a) |
callnumber |
QR1-502 |
title_auth |
Pleiotropic Actions of Aldehyde Reductase (AKR1A) |
abstract |
We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. |
abstractGer |
We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. |
abstract_unstemmed |
We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members. |
collection_details |
GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 |
container_issue |
6, p 343 |
title_short |
Pleiotropic Actions of Aldehyde Reductase (AKR1A) |
url |
https://doi.org/10.3390/metabo11060343 https://doaj.org/article/9db845b68e3547c69aa8797874e244f4 https://www.mdpi.com/2218-1989/11/6/343 https://doaj.org/toc/2218-1989 |
remote_bool |
true |
author2 |
Takujiro Homma Satoshi Miyata Motoko Takahashi |
author2Str |
Takujiro Homma Satoshi Miyata Motoko Takahashi |
ppnlink |
718627164 |
callnumber-subject |
QR - Microbiology |
mediatype_str_mv |
c |
isOA_txt |
true |
hochschulschrift_bool |
false |
doi_str |
10.3390/metabo11060343 |
callnumber-a |
QR1-502 |
up_date |
2024-07-03T22:57:10.344Z |
_version_ |
1803600454324584448 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ016784510</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240412180143.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2021 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3390/metabo11060343</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ016784510</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ9db845b68e3547c69aa8797874e244f4</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QR1-502</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Junichi Fujii</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Pleiotropic Actions of Aldehyde Reductase (AKR1A)</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">We provide an overview of the physiological roles of aldehyde reductase (AKR1A) and also discuss the functions of aldose reductase (AKR1B) and other family members when necessary. Many types of aldehyde compounds are cytotoxic and some are even carcinogenic. Such toxic aldehydes are detoxified via the action of AKR in an NADPH-dependent manner and the resulting products may exert anti-diabetic and anti-tumorigenic activity. AKR1A is capable of reducing 3-deoxyglucosone and methylglyoxal, which are reactive intermediates that are involved in glycation, a non-enzymatic glycosylation reaction. Accordingly, AKR1A is thought to suppress the formation of advanced glycation end products (AGEs) and prevent diabetic complications. AKR1A and, in part, AKR1B are responsible for the conversion of <span style="font-variant: small-caps;"<d</span<-glucuronate to <span style="font-variant: small-caps;"<l</span<-gulonate which constitutes a process for ascorbate (vitamin C) synthesis in competent animals. AKR1A is also involved in the reduction of <i<S</i<-nitrosylated glutathione and coenzyme A and thereby suppresses the protein <i<S</i<-nitrosylation that occurs under conditions in which the production of nitric oxide is stimulated. As the physiological functions of AKR1A are currently not completely understood, the genetic modification of <i<Akr1a</i< could reveal the latent functions of AKR1A and differentiate it from other family members.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<Akr1a</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a"><i<Akr1b</i<</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">reductive detoxification</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">glycation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ascorbate synthesis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">S-nitrosylation</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Microbiology</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Takujiro Homma</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Satoshi Miyata</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Motoko Takahashi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Metabolites</subfield><subfield code="d">MDPI AG, 2012</subfield><subfield code="g">11(2021), 6, p 343</subfield><subfield code="w">(DE-627)718627164</subfield><subfield code="w">(DE-600)2662251-8</subfield><subfield code="x">22181989</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:11</subfield><subfield code="g">year:2021</subfield><subfield code="g">number:6, p 343</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3390/metabo11060343</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/9db845b68e3547c69aa8797874e244f4</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://www.mdpi.com/2218-1989/11/6/343</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">https://doaj.org/toc/2218-1989</subfield><subfield code="y">Journal toc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_DOAJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">11</subfield><subfield code="j">2021</subfield><subfield code="e">6, p 343</subfield></datafield></record></collection>
|
score |
7.3974257 |