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Article: JUN

Zhang, Ming / Xu, Pei / Sun, Xiaolin / Zhang, Chen / Shi, Xiang / Li, Jancheng / Jiang, Jingyi / Chen, Chen / Zhang, Yani / Chen, Guohong / Li, Bichun / Zuo, Qisheng

Cytotechnology

2021 Volume 73, Issue 1, Page(s) 101–113

Abstract: The sex determination and control of poultry is a key problem in production and scientific research despite few studies on regulatory factors, especially transcription factors in sex determination. In the early stage of this study, high-throughput ... ...

Abstract	The sex determination and control of poultry is a key problem in production and scientific research despite few studies on regulatory factors, especially transcription factors in sex determination. In the early stage of this study, high-throughput sequencing was used to screen the differentially expressed gene
Language	English
Publishing date	2021-01-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	1035772-5
ISSN	0920-9069
ISSN	0920-9069
DOI	10.1007/s10616-020-00447-y
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Article ; Online: c-Jun NH

Chen, Yiping / Liu, Kaihua / Zhang, Jingwen / Hai, Yan / Wang, Peng / Wang, Hongyan / Liu, Qiuyan / Wong, Catherine C L / Yao, Jun / Gao, Yang / Liao, Yijiao / Tang, Xiuwen / Wang, Xiu Jun

Hepatology (Baltimore, Md.)

2020 Volume 71, Issue 5, Page(s) 1787–1801

Abstract: ... While the activation of c-Jun NH: Approach and results: In this study, we demonstrated that the activation of JNK ...

Abstract	Background and aims: Acetaminophen (APAP) overdose induces severe liver injury and hepatic failure. While the activation of c-Jun NH Approach and results: In this study, we demonstrated that the activation of JNK in mouse liver following exposure to APAP was correlated with the phosphorylation of Nrf2 and down-regulation of the antioxidant response element (ARE)-driven genes, NAD(P)H:quinone dehydrogenase 1, glutathione S-transferase α3, glutathione S-transferase M1, glutathione S-transferase M5, and aldo-keto reductase 1C. The JNK inhibitor, SP600125, or knockdown of JNK by infection of adenovirus expressing JNK small interfering RNA, ameliorated the APAP induced liver toxicity, and inhibited the phosphorylation of Nrf2 and down-regulation of detoxifying enzymes by stabilizing the transcription factor. Mechanistically, JNK antagonized Nrf2- and ARE-driven gene expression in a Kelch-like ECH-associated protein 1-independent manner. Biochemical analysis revealed that phosphorylated JNK (P-JNK) directly interacted with the Nrf2-ECH homology (Neh) 1 domain of Nrf2 and phosphorylated the serine-aspartate-serine motif 1 (SDS1) region in the Neh6 domain of Nrf2. Conclusions: Mass spectrometric analysis identified serine 335 in the SDS1 region of mNrf2 as the major phosphorylation site for modulation of Nrf2 ubiquitylation by P-JNK. This study demonstrates that Nrf2 is a target of P-JNK in AILI. Our finding may provide a strategy for the treatment of AILI.
MeSH term(s)	Acetaminophen/toxicity ; Analgesics, Non-Narcotic/toxicity ; Animals ; Anthracenes/pharmacology ; Chemical and Drug Induced Liver Injury/genetics ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/pathology ; Cytoprotection/drug effects ; Cytoprotection/genetics ; Disease Models, Animal ; Down-Regulation ; Enzyme Inhibitors/pharmacology ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 8/metabolism ; NF-E2-Related Factor 2 ; Phosphorylation/drug effects ; Protein Domains ; Ubiquitination
Chemical Substances	Analgesics, Non-Narcotic ; Anthracenes ; Enzyme Inhibitors ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; pyrazolanthrone (1TW30Y2766) ; Acetaminophen (362O9ITL9D) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24)
Language	English
Publishing date	2020-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.31116
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Zs.A 1660: Show issues

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Article: c-Jun as a one-way valve at the naive to primed interface.

Li, Dongwei / Luo, Ling / Guo, Lin / Wu, Chuman / Zhang, Ran / Peng, Yuling / Wu, Menghua / Kuang, Junqi / Li, Yan / Zhang, Yudan / Xie, Jun / Xie, Wenxiu / Mao, Rui / Ma, Gang / Fu, Xiuling / Chen, Jiekai / Hutchins, Andrew P / Pei, Duanqing

Cell & bioscience

2023 Volume 13, Issue 1, Page(s) 191

Abstract: Background: c-Jun is a proto-oncogene functioning as a transcription factor to activate gene ... However, its role in early embryonic development remains unknown.: Results: Here, we show that c-Jun acts ... as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced ...

Abstract	Background: c-Jun is a proto-oncogene functioning as a transcription factor to activate gene expression under many physiological and pathological conditions, particularly in somatic cells. However, its role in early embryonic development remains unknown. Results: Here, we show that c-Jun acts as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during the naive to primed transition, and it works to stabilize the chromatin structure and inhibit the reverse transition. Loss of c-Jun has surprisingly little effect on the naïve to primed transition, and no phenotypic effect on primed cells, however, in primed cells the loss of c-Jun leads to a failure to correctly close naïve-specific enhancers. When the primed cells are induced to reprogram to a naïve state, these enhancers are more rapidly activated when c-Jun is lost or impaired, and the conversion is more efficient. Conclusions: The results of this study indicate that c-Jun can function as a chromatin stabilizer in primed EpiSCs, to maintain the epigenetic cell type state and act as a one-way valve for cell fate conversions.
Language	English
Publishing date	2023-10-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2593367-X
ISSN	2045-3701
ISSN	2045-3701
DOI	10.1186/s13578-023-01141-0
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Article ; Online: The chromatin remodeling factor Arid1a cooperates with Jun/Fos to promote osteoclastogenesis by epigenetically upregulating Siglec15 expression.

Zhang, Yongxing / Sun, Hangxiang / Huang, Fei / Chen, Yang / Ding, Xiying / Zhou, Chenhe / Wu, Yan / Zhang, Qing / Ma, Xiao / Wang, Jun / Yue, Rui / Shen, Li / Sun, Xuxu / Ye, Zhaoming

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2024

Abstract: ... Siglec15) by transcription factor Jun/Fos, which results in the upregulation of Siglec15 and promotion ...

Abstract	Osteoporosis is characterized by an imbalance between osteoclast-mediated bone resorption and osteoblast-related bone formation, particularly increased osteoclastogenesis. However, the mechanisms by which epigenetic factors regulate osteoclast precursor differentiation during osteoclastogenesis remain poorly understood. Here, we show that the specific knockout of the chromatin remodeling factor Arid1a in bone marrow-derived macrophages (BMDMs) results in increased bone mass. The loss of Arid1a in BMDM inhibits cell-cell fusion and maturation of osteoclast precursors, thereby suppressing osteoclast differentiation. Mechanistically, Arid1a increases the chromatin access in the gene promoter region of sialic acid-binding Ig-like lectin 15 (Siglec15) by transcription factor Jun/Fos, which results in the upregulation of Siglec15 and promotion of osteoclast differentiation. However, the loss of Arid1a reprograms the chromatin structure to restrict Siglec15 expression in osteoclast precursors, thereby inhibiting BMDM differentiation into mature osteoclasts. Deleting Arid1a after ovariectomy (a model for postmenopausal bone loss) alleviated bone loss and maintained bone mass. In summary, epigenetic reprogramming mediated by Arid1a loss suppresses osteoclast differentiation and may serve as a promising therapeutic strategy for treating bone loss diseases.
Language	English
Publishing date	2024-03-11
Publishing country	England
Document type	Journal Article
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1093/jbmr/zjae042
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Zs.A 2142: Show issues

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Article ; Online: c-JUN is a barrier in hESC to cardiomyocyte transition.

Zhong, Hui / Zhang, Ran / Li, Guihuan / Huang, Ping / Zhang, Yudan / Zhu, Jieying / Kuang, Junqi / Hutchins, Andrew P / Qin, Dajiang / Zhu, Ping / Pei, Duanqing / Li, Dongwei

Life science alliance

2023 Volume 6, Issue 11

Abstract: Loss of c-JUN leads to early mouse embryonic death, possibly because of a failure to develop ... a normal cardiac system. How c-JUN regulates human cardiomyocyte cell fate remains unknown. Here, we used ... the in vitro differentiation of human pluripotent stem cells into cardiomyocytes to study the role of c-JUN ...

Abstract	Loss of c-JUN leads to early mouse embryonic death, possibly because of a failure to develop a normal cardiac system. How c-JUN regulates human cardiomyocyte cell fate remains unknown. Here, we used the in vitro differentiation of human pluripotent stem cells into cardiomyocytes to study the role of c-JUN. Surprisingly, the knockout of c-JUN improved cardiomyocyte generation, as determined by the number of TNNT2+ cells. ATAC-seq data showed that the c-JUN defect led to increased chromatin accessibility on critical regulatory elements related to cardiomyocyte development. ChIP-seq data showed that the knockout c-JUN increased RBBP5 and SETD1B expression, leading to improved H3K4me3 deposition on key genes that regulate cardiogenesis. The c-JUN KO phenotype could be copied using the histone demethylase inhibitor CPI-455, which also up-regulated H3K4me3 levels and increased cardiomyocyte generation. Single-cell RNA-seq data defined three cell branches, and knockout c-JUN activated more regulons that are related to cardiogenesis. In summary, our data demonstrated that c-JUN could regulate cardiomyocyte cell fate by modulating H3K4me3 modification and chromatin accessibility and shed light on how c-JUN regulates heart development in humans.
MeSH term(s)	Animals ; Humans ; Mice ; Cell Differentiation ; Chromatin/genetics ; Genes, jun ; Human Embryonic Stem Cells ; Myocytes, Cardiac ; Proto-Oncogene Proteins c-jun/metabolism
Chemical Substances	Chromatin ; JUN protein, human ; Proto-Oncogene Proteins c-jun
Language	English
Publishing date	2023-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202302121
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Article: USP5 facilitates bladder cancer progression by stabilizing the c-Jun protein.

Zhang, Hui-Hui / Zhang, An-Qi / Peng, Peng / Huang, Liang / Liu, Cai-Ying / Nie, Xin-Rui / Hou, De-Fu / Zhang, Xia / Li, Shang-Ze

Cancer cell international

2024 Volume 24, Issue 1, Page(s) 32

Abstract: ... and c-Jun. Cycloheximide (CHX) chase assays were performed to establish the effect of USP5 on c-Jun ... USP5 and c-Jun. USP5 was found to activate c-Jun by inhibiting its ubiquitination.: Conclusions ... Our results show that high USP5 expression promotes bladder cancer progression by stabilizing c-Jun and ...

Abstract	Background: Bladder cancer is the second most common genitourinary malignancy worldwide. The death rate of bladder cancer has increased every year. However, the molecular mechanism of bladder cancer is not sufficiently studied. Deubiquitinating enzymes (DUBs) play an important role in carcinogenesis. Several studies have demonstrated that USP5 associated with malignancy and pathological progression in hepatocellular carcinoma, colorectal and non-small cell lung cancer. However, the role of USP5 in bladder cancer need to be explored. Methods: The USP5 expression was analysed using the web server GEPIA. To explore USP5 function in bladder cancer, we constructed USP5-knockout cell lines in T24 cells. A FLAG-USP5 (WT USP5) plasmid and a plasmid FLAG-USP5 C335A (catalytic-inactive mutant) used to overexpress USP5 in EJ cells. CCK8, colony formation, transwell and scratch assays were used to assess cell viability, proliferation and migration. RNA sequencing (RNA-seq) and dual-luciferase reporter assays were performed to screen the pathway. Coimmunoprecipitation and immunofluorescence were used to explore the interaction between USP5 and c-Jun. Cycloheximide (CHX) chase assays were performed to establish the effect of USP5 on c-Jun stability. Xenograft mouse model was used to study the role of USP5 in bladder cancer. Results: USP5 expression is increased in bladder cancer patients. Genetic ablation of USP5 markedly inhibited bladder cancer cell proliferation, viability, and migration both in vitro and in vivo. RNA-seq and luciferase pathway screening showed that USP5 activated JNK signalling, and we identified the interaction between USP5 and c-Jun. USP5 was found to activate c-Jun by inhibiting its ubiquitination. Conclusions: Our results show that high USP5 expression promotes bladder cancer progression by stabilizing c-Jun and that USP5 is a potential therapeutic target in bladder cancer.
Language	English
Publishing date	2024-01-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-024-03222-7
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Article ; Online: Erratum: ZEGANG FENG, FENG ZHANG & JUN CHEN (2023) Cave-dwelling Neobisiidae in South China Karst, with descriptions of twelve new species of Bisetocreagris (Pseudoscorpiones, Neobisiidae) from Guizhou Province. Zootaxa, 5395 (1): 177.

Feng, Zegang / Zhang, Feng / Chen, Jun

Zootaxa

2024 Volume 5403, Issue 5, Page(s) 597–600

Language	English
Publishing date	2024-01-24
Publishing country	New Zealand
Document type	Journal Article
ISSN	1175-5334
ISSN (online)	1175-5334
DOI	10.11646/zootaxa.5403.5.7
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Article ; Online: c-Jun as a one-way valve at the naive to primed interface

Dongwei Li / Ling Luo / Lin Guo / Chuman Wu / Ran Zhang / Yuling Peng / Menghua Wu / Junqi Kuang / Yan Li / Yudan Zhang / Jun Xie / Wenxiu Xie / Rui Mao / Gang Ma / Xiuling Fu / Jiekai Chen / Andrew P. Hutchins / Duanqing Pei

Cell & Bioscience, Vol 13, Iss 1, Pp 1-

2023 Volume 16

Abstract: Abstract Background c-Jun is a proto-oncogene functioning as a transcription factor ... However, its role in early embryonic development remains unknown. Results Here, we show that c-Jun acts as a one-way ... valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during ...

Abstract	Abstract Background c-Jun is a proto-oncogene functioning as a transcription factor to activate gene expression under many physiological and pathological conditions, particularly in somatic cells. However, its role in early embryonic development remains unknown. Results Here, we show that c-Jun acts as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during the naive to primed transition, and it works to stabilize the chromatin structure and inhibit the reverse transition. Loss of c-Jun has surprisingly little effect on the naïve to primed transition, and no phenotypic effect on primed cells, however, in primed cells the loss of c-Jun leads to a failure to correctly close naïve-specific enhancers. When the primed cells are induced to reprogram to a naïve state, these enhancers are more rapidly activated when c-Jun is lost or impaired, and the conversion is more efficient. Conclusions The results of this study indicate that c-Jun can function as a chromatin stabilizer in primed EpiSCs, to maintain the epigenetic cell type state and act as a one-way valve for cell fate conversions.
Keywords	EpiSCs ; c-Jun ; Naïve to primed transition ; Primed to naïve transition ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: The role of c-Jun for beating cardiomycyte formation in prepared embryonic body.

Su, Lide / Zhang, Guofu / Jiang, Lili / Chi, Chao / Bai, Bing / Kang, Kai

Stem cell research & therapy

2023 Volume 14, Issue 1, Page(s) 371

Abstract: ... Jun serves as a cell cycle regulator for somatic cell fates, playing a key role in multiple molecular ... of c-Jun in promoting early-stage cardiac differentiation.: Methods: The c-Jun gene in mouse ... the resulting embryoid bodies. Cardiac differentiation was evaluated up to 9 days after c-Jun knockout (ko) via ...

Abstract	Background: Morbidity and mortality associated with cardiovascular diseases, such as myocardial infarction, stem from the inability of terminally differentiated cardiomyocytes to regenerate, and thus repair the damaged myocardial tissue structure. The molecular biological mechanisms behind the lack of regenerative capacity for those cardiomyocytes remains to be fully elucidated. Recent studies have shown that c-Jun serves as a cell cycle regulator for somatic cell fates, playing a key role in multiple molecular pathways, including the inhibition of cellular reprogramming, promoting angiogenesis, and aggravation of cardiac hypertrophy, but its role in cardiac development is largely unknown. This study aims to delineate the role of c-Jun in promoting early-stage cardiac differentiation. Methods: The c-Jun gene in mouse embryonic stem cells (mESCs) was knocked out with CRISPR-Cas9, and the hanging drop method used to prepare the resulting embryoid bodies. Cardiac differentiation was evaluated up to 9 days after c-Jun knockout (ko) via immunofluorescence, flow cytometric, and qPCR analyses. Results: Compared to the wild-type control group, obvious beating was observed among the c-Jun-ko mESCs after 6 days, which was also associated with significant increases in myocardial marker expression. Additionally, markers associated with mesoderm and endoderm cell layer development, essential for further differentiation of ESCs into cardiomyocytes, were also up-regulated in the c-Jun-ko cell group. Conclusions: Knocking out c-Jun directs ESCs toward a meso-endodermal cell lineage fate, in turn leading to generation of beating myocardial cells. Thus, c-Jun plays an important role in regulating early cardiac cell development.
MeSH term(s)	Animals ; Mice ; Cell Differentiation ; Cell Lineage ; Embryoid Bodies ; Mouse Embryonic Stem Cells ; Myocardium ; Myocytes, Cardiac/metabolism ; Proto-Oncogene Proteins c-jun/metabolism
Chemical Substances	Proto-Oncogene Proteins c-jun
Language	English
Publishing date	2023-12-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2548671-8
ISSN	1757-6512 ; 1757-6512
ISSN (online)	1757-6512
ISSN	1757-6512
DOI	10.1186/s13287-023-03544-9
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Article: Down-regulation of Jun induces senescence through destabilizing chromatin in osteoarthritis chondrocytes.

Xie, Ting / Ren, Xunshan / Zhuang, Huangming / Jiang, Fuze / Zhang, Yuelong / Zhou, Panghu

American journal of translational research

2023 Volume 15, Issue 7, Page(s) 4873–4886

Abstract: ... Using cytoHubba in Cytoscape, we identified Jun as the hub-ASDEG for OA chondrocytes. We confirmed ... the downregulation of Jun in OA rats and senescent chondrocytes by immunohistochemistry and quantitative ... were observed in chondrocytes treated with siRNA against Jun. Mechanistically, we observed micronuclei ...

Abstract	Objective: Osteoarthritis (OA) is the most common degenerative joint disease leading to disability worldwide. Cellular senescence is considered to be a fundamental pathogenic mechanism in the development of OA and has attracted increasing attention. However, regulatory mechanisms underlying chondrocyte senescence in OA remain unclear. Methods: Bioinformatic methods were used to screen key genes. Immunohistochemistry and the quantitative reverse transcription polymerase chain reaction were used to evaluate gene expression. RNA intervention experiments were performed to explore the functions of key genes. Results: We used 494 aging-associated genes provided by the Aging Atlas to identify the co-expression modules associated with age and OA. Thirty age-associated differentially expressed genes (ASDEGs) were identified. Using cytoHubba in Cytoscape, we identified Jun as the hub-ASDEG for OA chondrocytes. We confirmed the downregulation of Jun in OA rats and senescent chondrocytes by immunohistochemistry and quantitative reverse transcription polymerase chain reaction, respectively. Inhibition of proliferation and accelerated senescence were observed in chondrocytes treated with siRNA against Jun. Mechanistically, we observed micronuclei formation and reduced expression of H3K9me3 and heterochromatin protein 1gamma in siRNA-Jun-treated chondrocytes, indicating that destabilization of chromatin occurred during this treatment. Conclusion: Jun plays a crucial role in OA development and causes senescence by destabilizing chromatin in chondrocytes. These findings provide new insights into OA progression and suggest promising therapeutic targets.
Language	English
Publishing date	2023-07-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2471058-1
ISSN	1943-8141
ISSN	1943-8141
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