CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching

Purpose: Fetal hemoglobin (HbF) upregulation is a mitigating factor in β-hemoglobinopathies therapy like β-thalassemia and sickle cell diseases. Finding molecular mechanisms and the key regulators responsible for globin switching could be helpful to develop effective ways to HbF upregulation. In our...
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Autor*in:	Fatemeh Movahedi Motlagh [verfasserIn] Hamid Reza Soleimanpour‐Lichaei [verfasserIn] Mehdi Shamsara [verfasserIn] Azadeh Etemadzadeh [verfasserIn] Mohammad Hossein Modarressi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	crispr/cas9 beta hemoglobinopathies fetal hemoglobin globin switching bcl11a knockdown

Übergeordnetes Werk:	In: Advanced Pharmaceutical Bulletin - Tabriz University of Medical Sciences, 2011, 13(2023), 4, Seite 799-805
Übergeordnetes Werk:	volume:13 ; year:2023 ; number:4 ; pages:799-805

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.34172/apb.2023.074

Katalog-ID:	DOAJ098739875

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allfields	10.34172/apb.2023.074 doi (DE-627)DOAJ098739875 (DE-599)DOAJea27f757afe940d7abc57a8880829026 DE-627 ger DE-627 rakwb eng RM1-950 Fatemeh Movahedi Motlagh verfasserin aut CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Fetal hemoglobin (HbF) upregulation is a mitigating factor in β-hemoglobinopathies therapy like β-thalassemia and sickle cell diseases. Finding molecular mechanisms and the key regulators responsible for globin switching could be helpful to develop effective ways to HbF upregulation. In our prior in silico report, we identified a few factors that are likely to be responsible for globin switching. The goal of this study is to experimentally validate the factors. Methods: We established K562 cell line with BCL11A knock down leading to increase in HBG1/2 using CRISPR/Cas9 system. Then, using quantitative polymerase chain reaction (qPCR), we determined the expression level of the factors which were previously identified in our prior in silico study. Results: our analysis showed that BCL11A was substantially knocked down, resulting in the upregulation of HBG1/2 in the BCL11A-ablated K562 cells using CRISPR/Cas9 system. Additionally, the experimental data acquired in this study validated our prior bioinformatics findings about three potentially responsible genes for globin switching, namely HIST1H2Bl, TRIM58, and Al133243.2. Conclusion: BCL11A is a promising candidate for the treatment of β-hemoglobinopathies, with high HbF reactivation. In addition, HIST1H2BL, TRIM58 and Al133243.2 are likely to be involved in the mechanism of hemoglobin switching. To further validate the selected genes, more experimental in vivo and in vitro studies are required. crispr/cas9 beta hemoglobinopathies fetal hemoglobin globin switching bcl11a knockdown Therapeutics. Pharmacology Hamid Reza Soleimanpour‐Lichaei verfasserin aut Mehdi Shamsara verfasserin aut Azadeh Etemadzadeh verfasserin aut Mohammad Hossein Modarressi verfasserin aut In Advanced Pharmaceutical Bulletin Tabriz University of Medical Sciences, 2011 13(2023), 4, Seite 799-805 (DE-627)169603163X 22517308 nnns volume:13 year:2023 number:4 pages:799-805 https://doi.org/10.34172/apb.2023.074 kostenfrei https://doaj.org/article/ea27f757afe940d7abc57a8880829026 kostenfrei https://apb.tbzmed.ac.ir/PDF/apb-13-799.pdf kostenfrei https://doaj.org/toc/2228-5881 Journal toc kostenfrei https://doaj.org/toc/2251-7308 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 13 2023 4 799-805
spelling	10.34172/apb.2023.074 doi (DE-627)DOAJ098739875 (DE-599)DOAJea27f757afe940d7abc57a8880829026 DE-627 ger DE-627 rakwb eng RM1-950 Fatemeh Movahedi Motlagh verfasserin aut CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Fetal hemoglobin (HbF) upregulation is a mitigating factor in β-hemoglobinopathies therapy like β-thalassemia and sickle cell diseases. Finding molecular mechanisms and the key regulators responsible for globin switching could be helpful to develop effective ways to HbF upregulation. In our prior in silico report, we identified a few factors that are likely to be responsible for globin switching. The goal of this study is to experimentally validate the factors. Methods: We established K562 cell line with BCL11A knock down leading to increase in HBG1/2 using CRISPR/Cas9 system. Then, using quantitative polymerase chain reaction (qPCR), we determined the expression level of the factors which were previously identified in our prior in silico study. Results: our analysis showed that BCL11A was substantially knocked down, resulting in the upregulation of HBG1/2 in the BCL11A-ablated K562 cells using CRISPR/Cas9 system. Additionally, the experimental data acquired in this study validated our prior bioinformatics findings about three potentially responsible genes for globin switching, namely HIST1H2Bl, TRIM58, and Al133243.2. Conclusion: BCL11A is a promising candidate for the treatment of β-hemoglobinopathies, with high HbF reactivation. In addition, HIST1H2BL, TRIM58 and Al133243.2 are likely to be involved in the mechanism of hemoglobin switching. To further validate the selected genes, more experimental in vivo and in vitro studies are required. crispr/cas9 beta hemoglobinopathies fetal hemoglobin globin switching bcl11a knockdown Therapeutics. Pharmacology Hamid Reza Soleimanpour‐Lichaei verfasserin aut Mehdi Shamsara verfasserin aut Azadeh Etemadzadeh verfasserin aut Mohammad Hossein Modarressi verfasserin aut In Advanced Pharmaceutical Bulletin Tabriz University of Medical Sciences, 2011 13(2023), 4, Seite 799-805 (DE-627)169603163X 22517308 nnns volume:13 year:2023 number:4 pages:799-805 https://doi.org/10.34172/apb.2023.074 kostenfrei https://doaj.org/article/ea27f757afe940d7abc57a8880829026 kostenfrei https://apb.tbzmed.ac.ir/PDF/apb-13-799.pdf kostenfrei https://doaj.org/toc/2228-5881 Journal toc kostenfrei https://doaj.org/toc/2251-7308 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 13 2023 4 799-805
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allfieldsSound	10.34172/apb.2023.074 doi (DE-627)DOAJ098739875 (DE-599)DOAJea27f757afe940d7abc57a8880829026 DE-627 ger DE-627 rakwb eng RM1-950 Fatemeh Movahedi Motlagh verfasserin aut CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Fetal hemoglobin (HbF) upregulation is a mitigating factor in β-hemoglobinopathies therapy like β-thalassemia and sickle cell diseases. Finding molecular mechanisms and the key regulators responsible for globin switching could be helpful to develop effective ways to HbF upregulation. In our prior in silico report, we identified a few factors that are likely to be responsible for globin switching. The goal of this study is to experimentally validate the factors. Methods: We established K562 cell line with BCL11A knock down leading to increase in HBG1/2 using CRISPR/Cas9 system. Then, using quantitative polymerase chain reaction (qPCR), we determined the expression level of the factors which were previously identified in our prior in silico study. Results: our analysis showed that BCL11A was substantially knocked down, resulting in the upregulation of HBG1/2 in the BCL11A-ablated K562 cells using CRISPR/Cas9 system. Additionally, the experimental data acquired in this study validated our prior bioinformatics findings about three potentially responsible genes for globin switching, namely HIST1H2Bl, TRIM58, and Al133243.2. Conclusion: BCL11A is a promising candidate for the treatment of β-hemoglobinopathies, with high HbF reactivation. In addition, HIST1H2BL, TRIM58 and Al133243.2 are likely to be involved in the mechanism of hemoglobin switching. To further validate the selected genes, more experimental in vivo and in vitro studies are required. crispr/cas9 beta hemoglobinopathies fetal hemoglobin globin switching bcl11a knockdown Therapeutics. Pharmacology Hamid Reza Soleimanpour‐Lichaei verfasserin aut Mehdi Shamsara verfasserin aut Azadeh Etemadzadeh verfasserin aut Mohammad Hossein Modarressi verfasserin aut In Advanced Pharmaceutical Bulletin Tabriz University of Medical Sciences, 2011 13(2023), 4, Seite 799-805 (DE-627)169603163X 22517308 nnns volume:13 year:2023 number:4 pages:799-805 https://doi.org/10.34172/apb.2023.074 kostenfrei https://doaj.org/article/ea27f757afe940d7abc57a8880829026 kostenfrei https://apb.tbzmed.ac.ir/PDF/apb-13-799.pdf kostenfrei https://doaj.org/toc/2228-5881 Journal toc kostenfrei https://doaj.org/toc/2251-7308 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 13 2023 4 799-805
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callnumber-first	R - Medicine
author	Fatemeh Movahedi Motlagh
spellingShingle	Fatemeh Movahedi Motlagh misc RM1-950 misc crispr/cas9 misc beta hemoglobinopathies misc fetal hemoglobin misc globin switching misc bcl11a knockdown misc Therapeutics. Pharmacology CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching
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topic_title	RM1-950 CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching crispr/cas9 beta hemoglobinopathies fetal hemoglobin globin switching bcl11a knockdown
topic	misc RM1-950 misc crispr/cas9 misc beta hemoglobinopathies misc fetal hemoglobin misc globin switching misc bcl11a knockdown misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc crispr/cas9 misc beta hemoglobinopathies misc fetal hemoglobin misc globin switching misc bcl11a knockdown misc Therapeutics. Pharmacology
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title	CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching
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title_full	CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching
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author_browse	Fatemeh Movahedi Motlagh Hamid Reza Soleimanpour‐Lichaei Mehdi Shamsara Azadeh Etemadzadeh Mohammad Hossein Modarressi
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title_sort	crispr/cas9 ablated bcl11a unveils the genes with possible role of globin switching
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title_auth	CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching
abstract	Purpose: Fetal hemoglobin (HbF) upregulation is a mitigating factor in β-hemoglobinopathies therapy like β-thalassemia and sickle cell diseases. Finding molecular mechanisms and the key regulators responsible for globin switching could be helpful to develop effective ways to HbF upregulation. In our prior in silico report, we identified a few factors that are likely to be responsible for globin switching. The goal of this study is to experimentally validate the factors. Methods: We established K562 cell line with BCL11A knock down leading to increase in HBG1/2 using CRISPR/Cas9 system. Then, using quantitative polymerase chain reaction (qPCR), we determined the expression level of the factors which were previously identified in our prior in silico study. Results: our analysis showed that BCL11A was substantially knocked down, resulting in the upregulation of HBG1/2 in the BCL11A-ablated K562 cells using CRISPR/Cas9 system. Additionally, the experimental data acquired in this study validated our prior bioinformatics findings about three potentially responsible genes for globin switching, namely HIST1H2Bl, TRIM58, and Al133243.2. Conclusion: BCL11A is a promising candidate for the treatment of β-hemoglobinopathies, with high HbF reactivation. In addition, HIST1H2BL, TRIM58 and Al133243.2 are likely to be involved in the mechanism of hemoglobin switching. To further validate the selected genes, more experimental in vivo and in vitro studies are required.
abstractGer	Purpose: Fetal hemoglobin (HbF) upregulation is a mitigating factor in β-hemoglobinopathies therapy like β-thalassemia and sickle cell diseases. Finding molecular mechanisms and the key regulators responsible for globin switching could be helpful to develop effective ways to HbF upregulation. In our prior in silico report, we identified a few factors that are likely to be responsible for globin switching. The goal of this study is to experimentally validate the factors. Methods: We established K562 cell line with BCL11A knock down leading to increase in HBG1/2 using CRISPR/Cas9 system. Then, using quantitative polymerase chain reaction (qPCR), we determined the expression level of the factors which were previously identified in our prior in silico study. Results: our analysis showed that BCL11A was substantially knocked down, resulting in the upregulation of HBG1/2 in the BCL11A-ablated K562 cells using CRISPR/Cas9 system. Additionally, the experimental data acquired in this study validated our prior bioinformatics findings about three potentially responsible genes for globin switching, namely HIST1H2Bl, TRIM58, and Al133243.2. Conclusion: BCL11A is a promising candidate for the treatment of β-hemoglobinopathies, with high HbF reactivation. In addition, HIST1H2BL, TRIM58 and Al133243.2 are likely to be involved in the mechanism of hemoglobin switching. To further validate the selected genes, more experimental in vivo and in vitro studies are required.
abstract_unstemmed	Purpose: Fetal hemoglobin (HbF) upregulation is a mitigating factor in β-hemoglobinopathies therapy like β-thalassemia and sickle cell diseases. Finding molecular mechanisms and the key regulators responsible for globin switching could be helpful to develop effective ways to HbF upregulation. In our prior in silico report, we identified a few factors that are likely to be responsible for globin switching. The goal of this study is to experimentally validate the factors. Methods: We established K562 cell line with BCL11A knock down leading to increase in HBG1/2 using CRISPR/Cas9 system. Then, using quantitative polymerase chain reaction (qPCR), we determined the expression level of the factors which were previously identified in our prior in silico study. Results: our analysis showed that BCL11A was substantially knocked down, resulting in the upregulation of HBG1/2 in the BCL11A-ablated K562 cells using CRISPR/Cas9 system. Additionally, the experimental data acquired in this study validated our prior bioinformatics findings about three potentially responsible genes for globin switching, namely HIST1H2Bl, TRIM58, and Al133243.2. Conclusion: BCL11A is a promising candidate for the treatment of β-hemoglobinopathies, with high HbF reactivation. In addition, HIST1H2BL, TRIM58 and Al133243.2 are likely to be involved in the mechanism of hemoglobin switching. To further validate the selected genes, more experimental in vivo and in vitro studies are required.
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title_short	CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching
url	https://doi.org/10.34172/apb.2023.074 https://doaj.org/article/ea27f757afe940d7abc57a8880829026 https://apb.tbzmed.ac.ir/PDF/apb-13-799.pdf https://doaj.org/toc/2228-5881 https://doaj.org/toc/2251-7308
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up_date	2024-07-03T18:56:03.714Z
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Additionally, the experimental data acquired in this study validated our prior bioinformatics findings about three potentially responsible genes for globin switching, namely HIST1H2Bl, TRIM58, and Al133243.2. Conclusion: BCL11A is a promising candidate for the treatment of β-hemoglobinopathies, with high HbF reactivation. In addition, HIST1H2BL, TRIM58 and Al133243.2 are likely to be involved in the mechanism of hemoglobin switching. 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CRISPR/Cas9 Ablated BCL11A Unveils the Genes with Possible Role of Globin Switching

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