Tsc1 controls the development and function of alveolar macrophages
Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused ineffici...
Ausführliche Beschreibung
Autor*in: |
Chen, Song [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2018transfer abstract |
---|
Schlagwörter: |
---|
Umfang: |
5 |
---|
Übergeordnetes Werk: |
Enthalten in: Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag - Zhang, Zhikun ELSEVIER, 2019, BBRC, Orlando, Fla |
---|---|
Übergeordnetes Werk: |
volume:498 ; year:2018 ; number:3 ; day:6 ; month:04 ; pages:592-596 ; extent:5 |
Links: |
---|
DOI / URN: |
10.1016/j.bbrc.2018.03.027 |
---|
Katalog-ID: |
ELV042414830 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | ELV042414830 | ||
003 | DE-627 | ||
005 | 20230626001335.0 | ||
007 | cr uuu---uuuuu | ||
008 | 180726s2018 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1016/j.bbrc.2018.03.027 |2 doi | |
028 | 5 | 2 | |a GBV00000000000537.pica |
035 | |a (DE-627)ELV042414830 | ||
035 | |a (ELSEVIER)S0006-291X(18)30501-1 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
082 | 0 | 4 | |a 670 |q VZ |
084 | |a 51.60 |2 bkl | ||
084 | |a 58.45 |2 bkl | ||
100 | 1 | |a Chen, Song |e verfasserin |4 aut | |
245 | 1 | 0 | |a Tsc1 controls the development and function of alveolar macrophages |
264 | 1 | |c 2018transfer abstract | |
300 | |a 5 | ||
336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
337 | |a nicht spezifiziert |b z |2 rdamedia | ||
338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
520 | |a Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. | ||
520 | |a Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. | ||
650 | 7 | |a Function |2 Elsevier | |
650 | 7 | |a Development |2 Elsevier | |
650 | 7 | |a Tsc1 |2 Elsevier | |
650 | 7 | |a Proliferation |2 Elsevier | |
650 | 7 | |a Alveolar macrophages |2 Elsevier | |
700 | 1 | |a Yang, Qiongmei |4 oth | |
700 | 1 | |a Liu, Jingru |4 oth | |
700 | 1 | |a Huang, Huifang |4 oth | |
700 | 1 | |a Shi, Mingxia |4 oth | |
700 | 1 | |a Feng, Xiaoming |4 oth | |
773 | 0 | 8 | |i Enthalten in |n Academic Press |a Zhang, Zhikun ELSEVIER |t Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |d 2019 |d BBRC |g Orlando, Fla |w (DE-627)ELV002811154 |
773 | 1 | 8 | |g volume:498 |g year:2018 |g number:3 |g day:6 |g month:04 |g pages:592-596 |g extent:5 |
856 | 4 | 0 | |u https://doi.org/10.1016/j.bbrc.2018.03.027 |3 Volltext |
912 | |a GBV_USEFLAG_U | ||
912 | |a GBV_ELV | ||
912 | |a SYSFLAG_U | ||
936 | b | k | |a 51.60 |j Keramische Werkstoffe |j Hartstoffe |x Werkstoffkunde |q VZ |
936 | b | k | |a 58.45 |j Gesteinshüttenkunde |q VZ |
951 | |a AR | ||
952 | |d 498 |j 2018 |e 3 |b 6 |c 0406 |h 592-596 |g 5 |
author_variant |
s c sc |
---|---|
matchkey_str |
chensongyangqiongmeiliujingruhuanghuifan:2018----:s1otoshdvlpetnfntooav |
hierarchy_sort_str |
2018transfer abstract |
bklnumber |
51.60 58.45 |
publishDate |
2018 |
allfields |
10.1016/j.bbrc.2018.03.027 doi GBV00000000000537.pica (DE-627)ELV042414830 (ELSEVIER)S0006-291X(18)30501-1 DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Chen, Song verfasserin aut Tsc1 controls the development and function of alveolar macrophages 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages Elsevier Yang, Qiongmei oth Liu, Jingru oth Huang, Huifang oth Shi, Mingxia oth Feng, Xiaoming oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:498 year:2018 number:3 day:6 month:04 pages:592-596 extent:5 https://doi.org/10.1016/j.bbrc.2018.03.027 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 498 2018 3 6 0406 592-596 5 |
spelling |
10.1016/j.bbrc.2018.03.027 doi GBV00000000000537.pica (DE-627)ELV042414830 (ELSEVIER)S0006-291X(18)30501-1 DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Chen, Song verfasserin aut Tsc1 controls the development and function of alveolar macrophages 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages Elsevier Yang, Qiongmei oth Liu, Jingru oth Huang, Huifang oth Shi, Mingxia oth Feng, Xiaoming oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:498 year:2018 number:3 day:6 month:04 pages:592-596 extent:5 https://doi.org/10.1016/j.bbrc.2018.03.027 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 498 2018 3 6 0406 592-596 5 |
allfields_unstemmed |
10.1016/j.bbrc.2018.03.027 doi GBV00000000000537.pica (DE-627)ELV042414830 (ELSEVIER)S0006-291X(18)30501-1 DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Chen, Song verfasserin aut Tsc1 controls the development and function of alveolar macrophages 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages Elsevier Yang, Qiongmei oth Liu, Jingru oth Huang, Huifang oth Shi, Mingxia oth Feng, Xiaoming oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:498 year:2018 number:3 day:6 month:04 pages:592-596 extent:5 https://doi.org/10.1016/j.bbrc.2018.03.027 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 498 2018 3 6 0406 592-596 5 |
allfieldsGer |
10.1016/j.bbrc.2018.03.027 doi GBV00000000000537.pica (DE-627)ELV042414830 (ELSEVIER)S0006-291X(18)30501-1 DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Chen, Song verfasserin aut Tsc1 controls the development and function of alveolar macrophages 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages Elsevier Yang, Qiongmei oth Liu, Jingru oth Huang, Huifang oth Shi, Mingxia oth Feng, Xiaoming oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:498 year:2018 number:3 day:6 month:04 pages:592-596 extent:5 https://doi.org/10.1016/j.bbrc.2018.03.027 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 498 2018 3 6 0406 592-596 5 |
allfieldsSound |
10.1016/j.bbrc.2018.03.027 doi GBV00000000000537.pica (DE-627)ELV042414830 (ELSEVIER)S0006-291X(18)30501-1 DE-627 ger DE-627 rakwb eng 670 VZ 51.60 bkl 58.45 bkl Chen, Song verfasserin aut Tsc1 controls the development and function of alveolar macrophages 2018transfer abstract 5 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages Elsevier Yang, Qiongmei oth Liu, Jingru oth Huang, Huifang oth Shi, Mingxia oth Feng, Xiaoming oth Enthalten in Academic Press Zhang, Zhikun ELSEVIER Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag 2019 BBRC Orlando, Fla (DE-627)ELV002811154 volume:498 year:2018 number:3 day:6 month:04 pages:592-596 extent:5 https://doi.org/10.1016/j.bbrc.2018.03.027 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 498 2018 3 6 0406 592-596 5 |
language |
English |
source |
Enthalten in Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag Orlando, Fla volume:498 year:2018 number:3 day:6 month:04 pages:592-596 extent:5 |
sourceStr |
Enthalten in Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag Orlando, Fla volume:498 year:2018 number:3 day:6 month:04 pages:592-596 extent:5 |
format_phy_str_mv |
Article |
bklname |
Keramische Werkstoffe Hartstoffe Gesteinshüttenkunde |
institution |
findex.gbv.de |
topic_facet |
Function Development Tsc1 Proliferation Alveolar macrophages |
dewey-raw |
670 |
isfreeaccess_bool |
false |
container_title |
Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |
authorswithroles_txt_mv |
Chen, Song @@aut@@ Yang, Qiongmei @@oth@@ Liu, Jingru @@oth@@ Huang, Huifang @@oth@@ Shi, Mingxia @@oth@@ Feng, Xiaoming @@oth@@ |
publishDateDaySort_date |
2018-01-06T00:00:00Z |
hierarchy_top_id |
ELV002811154 |
dewey-sort |
3670 |
id |
ELV042414830 |
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">ELV042414830</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626001335.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180726s2018 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.bbrc.2018.03.027</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000537.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV042414830</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0006-291X(18)30501-1</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="082" ind1="0" ind2="4"><subfield code="a">670</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">51.60</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">58.45</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Chen, Song</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Tsc1 controls the development and function of alveolar macrophages</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">5</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Function</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Development</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Tsc1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Proliferation</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Alveolar macrophages</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yang, Qiongmei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Jingru</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Huang, Huifang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shi, Mingxia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Feng, Xiaoming</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="a">Zhang, Zhikun ELSEVIER</subfield><subfield code="t">Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag</subfield><subfield code="d">2019</subfield><subfield code="d">BBRC</subfield><subfield code="g">Orlando, Fla</subfield><subfield code="w">(DE-627)ELV002811154</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:498</subfield><subfield code="g">year:2018</subfield><subfield code="g">number:3</subfield><subfield code="g">day:6</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:592-596</subfield><subfield code="g">extent:5</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.bbrc.2018.03.027</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">51.60</subfield><subfield code="j">Keramische Werkstoffe</subfield><subfield code="j">Hartstoffe</subfield><subfield code="x">Werkstoffkunde</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">58.45</subfield><subfield code="j">Gesteinshüttenkunde</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">498</subfield><subfield code="j">2018</subfield><subfield code="e">3</subfield><subfield code="b">6</subfield><subfield code="c">0406</subfield><subfield code="h">592-596</subfield><subfield code="g">5</subfield></datafield></record></collection>
|
author |
Chen, Song |
spellingShingle |
Chen, Song ddc 670 bkl 51.60 bkl 58.45 Elsevier Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages Tsc1 controls the development and function of alveolar macrophages |
authorStr |
Chen, Song |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV002811154 |
format |
electronic Article |
dewey-ones |
670 - Manufacturing |
delete_txt_mv |
keep |
author_role |
aut |
collection |
elsevier |
remote_str |
true |
illustrated |
Not Illustrated |
topic_title |
670 VZ 51.60 bkl 58.45 bkl Tsc1 controls the development and function of alveolar macrophages Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages Elsevier |
topic |
ddc 670 bkl 51.60 bkl 58.45 Elsevier Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages |
topic_unstemmed |
ddc 670 bkl 51.60 bkl 58.45 Elsevier Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages |
topic_browse |
ddc 670 bkl 51.60 bkl 58.45 Elsevier Function Elsevier Development Elsevier Tsc1 Elsevier Proliferation Elsevier Alveolar macrophages |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
zu |
author2_variant |
q y qy j l jl h h hh m s ms x f xf |
hierarchy_parent_title |
Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |
hierarchy_parent_id |
ELV002811154 |
dewey-tens |
670 - Manufacturing |
hierarchy_top_title |
Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |
isfreeaccess_txt |
false |
familylinks_str_mv |
(DE-627)ELV002811154 |
title |
Tsc1 controls the development and function of alveolar macrophages |
ctrlnum |
(DE-627)ELV042414830 (ELSEVIER)S0006-291X(18)30501-1 |
title_full |
Tsc1 controls the development and function of alveolar macrophages |
author_sort |
Chen, Song |
journal |
Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |
journalStr |
Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag |
lang_code |
eng |
isOA_bool |
false |
dewey-hundreds |
600 - Technology |
recordtype |
marc |
publishDateSort |
2018 |
contenttype_str_mv |
zzz |
container_start_page |
592 |
author_browse |
Chen, Song |
container_volume |
498 |
physical |
5 |
class |
670 VZ 51.60 bkl 58.45 bkl |
format_se |
Elektronische Aufsätze |
author-letter |
Chen, Song |
doi_str_mv |
10.1016/j.bbrc.2018.03.027 |
dewey-full |
670 |
title_sort |
tsc1 controls the development and function of alveolar macrophages |
title_auth |
Tsc1 controls the development and function of alveolar macrophages |
abstract |
Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. |
abstractGer |
Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. |
abstract_unstemmed |
Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs. |
collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
container_issue |
3 |
title_short |
Tsc1 controls the development and function of alveolar macrophages |
url |
https://doi.org/10.1016/j.bbrc.2018.03.027 |
remote_bool |
true |
author2 |
Yang, Qiongmei Liu, Jingru Huang, Huifang Shi, Mingxia Feng, Xiaoming |
author2Str |
Yang, Qiongmei Liu, Jingru Huang, Huifang Shi, Mingxia Feng, Xiaoming |
ppnlink |
ELV002811154 |
mediatype_str_mv |
z |
isOA_txt |
false |
hochschulschrift_bool |
false |
author2_role |
oth oth oth oth oth |
doi_str |
10.1016/j.bbrc.2018.03.027 |
up_date |
2024-07-06T22:44:16.174Z |
_version_ |
1803871433444556800 |
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">ELV042414830</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626001335.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180726s2018 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.bbrc.2018.03.027</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000537.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV042414830</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0006-291X(18)30501-1</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="082" ind1="0" ind2="4"><subfield code="a">670</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">51.60</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">58.45</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Chen, Song</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Tsc1 controls the development and function of alveolar macrophages</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">5</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Alveolar macrophages (AMs) are pivotal for maintaining the lung homeostasis, but how the development and function of AMs regulated remains largely unknown. In the present study, we demonstrated that the number of AMs was controlled by the Tsc1 protein. Cd11c-specific deletion of Tsc1 caused inefficient transition from pre-AMs to AMs in lung, which led to a great reduction of AM population. Ablation of Tsc1 downregulated the expression of surface marker CD64 and SiglecF on AMs. We further showed that conditional knockout of Tsc1 led to enhanced proliferation and increased reactive oxygen species (ROS) production and phagocytosis in AMs. These results indicated that Tsc1 was a critical regulator of development, proliferation and function in AMs.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Function</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Development</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Tsc1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Proliferation</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Alveolar macrophages</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yang, Qiongmei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Jingru</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Huang, Huifang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shi, Mingxia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Feng, Xiaoming</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="a">Zhang, Zhikun ELSEVIER</subfield><subfield code="t">Preparation and characterization of glass-ceramics via co-sintering of coal fly ash and oil shale ash-derived amorphous slag</subfield><subfield code="d">2019</subfield><subfield code="d">BBRC</subfield><subfield code="g">Orlando, Fla</subfield><subfield code="w">(DE-627)ELV002811154</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:498</subfield><subfield code="g">year:2018</subfield><subfield code="g">number:3</subfield><subfield code="g">day:6</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:592-596</subfield><subfield code="g">extent:5</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.bbrc.2018.03.027</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">51.60</subfield><subfield code="j">Keramische Werkstoffe</subfield><subfield code="j">Hartstoffe</subfield><subfield code="x">Werkstoffkunde</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">58.45</subfield><subfield code="j">Gesteinshüttenkunde</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">498</subfield><subfield code="j">2018</subfield><subfield code="e">3</subfield><subfield code="b">6</subfield><subfield code="c">0406</subfield><subfield code="h">592-596</subfield><subfield code="g">5</subfield></datafield></record></collection>
|
score |
7.399617 |