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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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Zs.A 2604: Show issues

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Article ; Online: Role of c-Jun NH

Niu, Xiao-Jing / Wang, Li-Jun / Meng, Hui / Wang, Hong-Fang / Xu, Bao-Hua / Wang, Chen

Insect science

2022 Volume 30, Issue 1, Page(s) 47–64

Abstract: ... stress responses. The function of the c-Jun NH ...

Abstract	The mitogen-activated protein kinase (MAPK) cascade pathway plays an important role in regulating stress responses. The function of the c-Jun NH
MeSH term(s)	Bees ; Animals ; Antioxidants/metabolism ; Transcription Factor AP-1 ; Mitogen-Activated Protein Kinases ; Pesticides ; Insect Proteins/genetics
Chemical Substances	Antioxidants ; Transcription Factor AP-1 ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Pesticides ; Insect Proteins
Language	English
Publishing date	2022-06-01
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2179775-4
ISSN	1744-7917 ; 1672-9609
ISSN (online)	1744-7917
ISSN	1672-9609
DOI	10.1111/1744-7917.13053
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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: A study related to the treatment of gastric cancer with Xiang-Sha-Liu-Jun-Zi-Tang based on network analysis.

Jiang, Ke / Liu, Heli / Ge, Jie / Yang, Bo / Wang, Yu / Wang, Wenbo / Wen, Yuqi / Zeng, Siqing / Chen, Quan / Huang, Jun / Xiong, Xingui

Heliyon

2023 Volume 9, Issue 9, Page(s) e19546

Abstract: Purpose: Xiang-Sha-Liu-Jun-Zi-Tang(XSLJZT) is a common formula for the treatment of Gastric Cancer ...

Abstract	Purpose: Xiang-Sha-Liu-Jun-Zi-Tang(XSLJZT) is a common formula for the treatment of Gastric Cancer(GC) and is widely used in clinical practice, however, there is a lack of investigation into its mechanism. Methods: We collected and organized drug and disease targets, constructed the "XSLJZT-Active Ingredient-Target" visualization network, and performed GO and KEGG functional enrichment analysis of crossover genes, followed by molecular docking of active ingredients and core targets. The best docked monomers were combined with weighted gene co-expression network analysis(WGCNA) and macroscopically analyzed by GO and KEGG enrichment techniques. The results of cluster gene difference analysis, ROC evaluation, and CIBERSORT immune infiltration analysis were evaluated and finally supported by cellular experiments. Results: The main components of XSLJZT are quercetin, stigmasterol, and naringenin, effectively treat GC by targeting STAT3, TP53 and MAPK3, which are involved in IL-17, TNF and HIF-1 signaling pathways. The results of molecular docking showed that quercetin bound better to the core targets. We performed an in-depth analysis of this monomer and found that quercetin acts on the core targets of TP53, MMP9, TIMP1 and MYC, and is involved in two key signaling pathways, TNF and IL-17, thus effectively treating GC. The experimental results are consistent with our analysis that quercetin inhibits the proliferation of GC cells and promotes apoptosis, and TP53, MYC and TIMP1 are the quercetin targets for the treatment of GC. Conclusion: The present study tentatively suggests that quercetin, the main active ingredient in XSLJZT, can exert a therapeutic effect on GC by targeting TIMP1.
Language	English
Publishing date	2023-08-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e19546
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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: Cooperation of MLL1 and Jun in controlling H3K4me3 on enhancers in colorectal cancer.

Lin, Xiang / Chen, Ji-Dong / Wang, Chen-Yu / Cai, Zhen / Zhan, Rui / Yang, Chen / Zhang, La-Ying / Li, Lian-Yun / Xiao, Yong / Chen, Ming-Kai / Wu, Min

Genome biology

2023 Volume 24, Issue 1, Page(s) 268

Abstract: ... on the identified Vm3Es. We demonstrate that the transcription factor AP1/JUN interacts with MLL1 and regulates m3E ...

Abstract	Background: Enhancer dysregulation is one of the important features for cancer cells. Enhancers enriched with H3K4me3 have been implicated to play important roles in cancer. However, their detailed features and regulatory mechanisms have not been well characterized. Results: Here, we profile the landscape of H3K4me3-enriched enhancers (m3Es) in 43 pairs of colorectal cancer (CRC) samples. M3Es are widely distributed in CRC and averagely possess around 10% of total active enhancers. We identify 1322 gain variant m3Es and 367 lost variant m3Es in CRC. The target genes of the gain m3Es are enriched in immune response pathways. We experimentally prove that repression of CBX8 and RPS6KA5 m3Es inhibits target gene expression in CRC. Furthermore, we find histone methyltransferase MLL1 is responsible for depositing H3K4me3 on the identified Vm3Es. We demonstrate that the transcription factor AP1/JUN interacts with MLL1 and regulates m3E activity. Application of a small chemical inhibitor for MLL1 activity, OICR-9429, represses target gene expression of the identified Vm3Es, enhances anti-tumor immunity and inhibits CRC growth in an animal model. Conclusions: Taken together, our study illustrates the genome-wide landscape and the regulatory mechanisms of m3Es in CRC, and reveals potential novel strategies for cancer treatment.
MeSH term(s)	Animals ; Colorectal Neoplasms/genetics ; Enhancer Elements, Genetic ; Histones/metabolism ; Myeloid-Lymphoid Leukemia Protein/genetics ; Myeloid-Lymphoid Leukemia Protein/metabolism ; Transcription Factor AP-1/metabolism ; Humans ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism
Chemical Substances	histone H3 trimethyl Lys4 ; Histones ; Myeloid-Lymphoid Leukemia Protein (149025-06-9) ; Transcription Factor AP-1 ; KMT2A protein, human ; JUN protein, human ; Proto-Oncogene Proteins c-jun
Language	English
Publishing date	2023-11-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-023-03108-3
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Article ; Online: TYRO3 protects podocyte via JNK/c-jun-P53 pathway.

Zhang, Liwen / Jiang, Song / Shi, Jinsong / Xu, Xiaodong / Wang, Ling / Zhai, Xiuwen / Hou, Qin / Qin, Weisong / Chen, Zhaohong

Archives of biochemistry and biophysics

2023 Volume 739, Page(s) 109578

Abstract: ... conferred antiapoptotic effects through the activation of JNK/c-jun-P53 in podocytes. Our results revealed ...

Abstract	Podocyte injury plays a critical role in diabetic kidney disease (DKD). Our previous work demonstrated a protective role of tyrosine-protein kinase receptor TYRO3 in glomerular disease; However, the downstream signaling of TYRO3 remains unclear. Our data showed that genetic ablation of tyro3 in zebrafish recapitulated a nephrotic syndrome phenotype. TYRO3 expression was suppressed by high glucose and TGF-β, which may contribute to the decreased TYRO3 expression in progressive DKD. Moreover, knockdown of TYRO3 expression with siRNA induced podocytes apoptosis and cytoskeleton rearrangement. Further study revealed that TYRO3 conferred antiapoptotic effects through the activation of JNK/c-jun-P53 in podocytes. Our results revealed a novel signaling module of TYRO3 in podocyte homeostasis, which provides a new molecular insight of TYRO3 effect in podocyte protection.
MeSH term(s)	Animals ; Podocytes/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Zebrafish/metabolism ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/metabolism ; Signal Transduction ; Apoptosis
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2023-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2023.109578
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