E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1

Apoptosis is a very important process of cell death controlled by multiple genes during which cells undergo certain events before dying. Apoptosis helps to clean the unnecessary cells and has critical physiological significance. Altered apoptosis results in a disorder of cell death and is associated...
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Autor*in:	Ge Yang [verfasserIn] Pin Wan [verfasserIn] Qi Xiang [verfasserIn] Shanyu Huang [verfasserIn] Siyu Huang [verfasserIn] Jun Wang [verfasserIn] Kailang Wu [verfasserIn] Jianguo Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	ankyrin repeat and SOCS box-containing 17, ASB17 apoptosis etoposide B-cell leukemia/lymphoma w, BCLW caspases myeloid cell leukemia-1, MCL1

Übergeordnetes Werk:	In: Biology - MDPI AG, 2012, 10(2021), 3, p 234
Übergeordnetes Werk:	volume:10 ; year:2021 ; number:3, p 234

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/biology10030234

Katalog-ID:	DOAJ062637320

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520			\|a Apoptosis is a very important process of cell death controlled by multiple genes during which cells undergo certain events before dying. Apoptosis helps to clean the unnecessary cells and has critical physiological significance. Altered apoptosis results in a disorder of cell death and is associated with many diseases such as neurodegenerative diseases and cancers. Here, we reported that the ankyrin repeat and SOCS box protein 17 (ASB17) was mainly expressed in the testis and promoted apoptosis both in vivo and in vitro. Analyzing ASB17-deficient mice generated by using the CRISPR/Cas9 system, we demonstrated that ASB17 deficiency resulted in the reduction of apoptosis in spermatogenic cells, but it did not affect the development of spermatozoa or normal fertility. Next, in an in vivo model, ASB17 deficiency prevented the apoptosis of spermatogonia induced by etoposide in male mice. We noted that ASB17 promoted apoptosis in a caspase-dependent manner in vitro. Moreover, ASB17 interacted with the members of the BCL2 family, including BCL2, BCLX, BCLW, and MCL1. Interestingly, ASB17 specifically degraded the two anti-apoptotic factors, BCLW and MCL1, in a ubiquitylation-dependent fashion. Collectively, our findings suggested that ASB17 acted as a distinct positive regulator of cell apoptosis.
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callnumber-first	Q - Science
author	Ge Yang
spellingShingle	Ge Yang misc QH301-705.5 misc ankyrin repeat and SOCS box-containing 17, ASB17 misc apoptosis misc etoposide misc B-cell leukemia/lymphoma w, BCLW misc caspases misc myeloid cell leukemia-1, MCL1 misc Biology (General) E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1
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topic_title	QH301-705.5 E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1 ankyrin repeat and SOCS box-containing 17, ASB17 apoptosis etoposide B-cell leukemia/lymphoma w, BCLW caspases myeloid cell leukemia-1, MCL1
topic	misc QH301-705.5 misc ankyrin repeat and SOCS box-containing 17, ASB17 misc apoptosis misc etoposide misc B-cell leukemia/lymphoma w, BCLW misc caspases misc myeloid cell leukemia-1, MCL1 misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc ankyrin repeat and SOCS box-containing 17, ASB17 misc apoptosis misc etoposide misc B-cell leukemia/lymphoma w, BCLW misc caspases misc myeloid cell leukemia-1, MCL1 misc Biology (General)
topic_browse	misc QH301-705.5 misc ankyrin repeat and SOCS box-containing 17, ASB17 misc apoptosis misc etoposide misc B-cell leukemia/lymphoma w, BCLW misc caspases misc myeloid cell leukemia-1, MCL1 misc Biology (General)
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title	E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1
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title_full	E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1
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author_browse	Ge Yang Pin Wan Qi Xiang Shanyu Huang Siyu Huang Jun Wang Kailang Wu Jianguo Wu
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title_sort	e3 ubiquitin ligase asb17 promotes apoptosis by ubiquitylating and degrading bclw and mcl1
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title_auth	E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1
abstract	Apoptosis is a very important process of cell death controlled by multiple genes during which cells undergo certain events before dying. Apoptosis helps to clean the unnecessary cells and has critical physiological significance. Altered apoptosis results in a disorder of cell death and is associated with many diseases such as neurodegenerative diseases and cancers. Here, we reported that the ankyrin repeat and SOCS box protein 17 (ASB17) was mainly expressed in the testis and promoted apoptosis both in vivo and in vitro. Analyzing ASB17-deficient mice generated by using the CRISPR/Cas9 system, we demonstrated that ASB17 deficiency resulted in the reduction of apoptosis in spermatogenic cells, but it did not affect the development of spermatozoa or normal fertility. Next, in an in vivo model, ASB17 deficiency prevented the apoptosis of spermatogonia induced by etoposide in male mice. We noted that ASB17 promoted apoptosis in a caspase-dependent manner in vitro. Moreover, ASB17 interacted with the members of the BCL2 family, including BCL2, BCLX, BCLW, and MCL1. Interestingly, ASB17 specifically degraded the two anti-apoptotic factors, BCLW and MCL1, in a ubiquitylation-dependent fashion. Collectively, our findings suggested that ASB17 acted as a distinct positive regulator of cell apoptosis.
abstractGer	Apoptosis is a very important process of cell death controlled by multiple genes during which cells undergo certain events before dying. Apoptosis helps to clean the unnecessary cells and has critical physiological significance. Altered apoptosis results in a disorder of cell death and is associated with many diseases such as neurodegenerative diseases and cancers. Here, we reported that the ankyrin repeat and SOCS box protein 17 (ASB17) was mainly expressed in the testis and promoted apoptosis both in vivo and in vitro. Analyzing ASB17-deficient mice generated by using the CRISPR/Cas9 system, we demonstrated that ASB17 deficiency resulted in the reduction of apoptosis in spermatogenic cells, but it did not affect the development of spermatozoa or normal fertility. Next, in an in vivo model, ASB17 deficiency prevented the apoptosis of spermatogonia induced by etoposide in male mice. We noted that ASB17 promoted apoptosis in a caspase-dependent manner in vitro. Moreover, ASB17 interacted with the members of the BCL2 family, including BCL2, BCLX, BCLW, and MCL1. Interestingly, ASB17 specifically degraded the two anti-apoptotic factors, BCLW and MCL1, in a ubiquitylation-dependent fashion. Collectively, our findings suggested that ASB17 acted as a distinct positive regulator of cell apoptosis.
abstract_unstemmed	Apoptosis is a very important process of cell death controlled by multiple genes during which cells undergo certain events before dying. Apoptosis helps to clean the unnecessary cells and has critical physiological significance. Altered apoptosis results in a disorder of cell death and is associated with many diseases such as neurodegenerative diseases and cancers. Here, we reported that the ankyrin repeat and SOCS box protein 17 (ASB17) was mainly expressed in the testis and promoted apoptosis both in vivo and in vitro. Analyzing ASB17-deficient mice generated by using the CRISPR/Cas9 system, we demonstrated that ASB17 deficiency resulted in the reduction of apoptosis in spermatogenic cells, but it did not affect the development of spermatozoa or normal fertility. Next, in an in vivo model, ASB17 deficiency prevented the apoptosis of spermatogonia induced by etoposide in male mice. We noted that ASB17 promoted apoptosis in a caspase-dependent manner in vitro. Moreover, ASB17 interacted with the members of the BCL2 family, including BCL2, BCLX, BCLW, and MCL1. Interestingly, ASB17 specifically degraded the two anti-apoptotic factors, BCLW and MCL1, in a ubiquitylation-dependent fashion. Collectively, our findings suggested that ASB17 acted as a distinct positive regulator of cell apoptosis.
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title_short	E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1
url	https://doi.org/10.3390/biology10030234 https://doaj.org/article/6d1a385df8f64f1c995367a524fd7853 https://www.mdpi.com/2079-7737/10/3/234 https://doaj.org/toc/2079-7737
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author2	Pin Wan Qi Xiang Shanyu Huang Siyu Huang Jun Wang Kailang Wu Jianguo Wu
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E3 Ubiquitin Ligase ASB17 Promotes Apoptosis by Ubiquitylating and Degrading BCLW and MCL1

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