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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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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
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: NOD2/c-Jun NH

Luo, Haixia / Wu, Xixi / Xu, Zhaokun / Hao, Xiujing / Wang, Yongyu / Li, Min

Journal of bacteriology

2020 Volume 202, Issue 20

Abstract: Mycoplasma ... ...

Abstract	Mycoplasma ovipneumoniae
MeSH term(s)	Animals ; Autophagy ; MAP Kinase Signaling System ; Macrophages/microbiology ; Mice ; Mycoplasma ovipneumoniae/pathogenicity ; Nod2 Signaling Adaptor Protein/metabolism ; Phosphorylation ; RAW 264.7 Cells
Chemical Substances	Nod2 Signaling Adaptor Protein ; Nod2 protein, mouse
Language	English
Publishing date	2020-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2968-3
ISSN	1098-5530 ; 0021-9193
ISSN (online)	1098-5530
ISSN	0021-9193
DOI	10.1128/JB.00689-19
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Article ; Online: Reprogramming Stars #7: Dynamic Pluripotent Stem Cell States and Their Applications-An Interview with Dr. Jun Wu.

Wu, Jun / Pereira, Carlos-Filipe / Lu, Yuancheng Ryan

Cellular reprogramming

2022 Volume 24, Issue 3, Page(s) 105–110

MeSH term(s)	Cell Differentiation ; Cellular Reprogramming ; Induced Pluripotent Stem Cells ; Pluripotent Stem Cells
Language	English
Publishing date	2022-05-14
Publishing country	United States
Document type	Interview
ZDB-ID	2542436-1
ISSN	2152-4998 ; 1557-7457 ; 2152-4971
ISSN (online)	2152-4998 ; 1557-7457
ISSN	2152-4971
DOI	10.1089/cell.2022.29064.jc
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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: c-Jun N-terminal kinase signaling in cellular senescence.

Deng, Ying / Adam, Vojtech / Nepovimova, Eugenie / Heger, Zbynek / Valko, Marian / Wu, Qinghua / Wei, Wei / Kuca, Kamil

Archives of toxicology

2023 Volume 97, Issue 8, Page(s) 2089–2109

Abstract: ... not fully understood. Emerging evidence has indicated that c-Jun N-terminal kinase (JNK) signaling is ...

Abstract	Cellular senescence leads to decreased tissue regeneration and inflammation and is associated with diabetes, neurodegenerative diseases, and tumorigenesis. However, the mechanisms of cellular senescence are not fully understood. Emerging evidence has indicated that c-Jun N-terminal kinase (JNK) signaling is involved in the regulation of cellular senescence. JNK can downregulate hypoxia inducible factor-1α to accelerate hypoxia-induced neuronal cell senescence. The activation of JNK inhibits mTOR activity and triggers autophagy, which promotes cellular senescence. JNK can upregulate the expression of p53 and Bcl-2 and accelerates cancer cell senescence; however, this signaling also mediates the expression of amphiregulin and PD-LI to achieve cancer cell immune evasion and prevents their senescence. The activation of JNK further triggers forkhead box O expression and its target gene Jafrac1 to extend the lifespan of Drosophila. JNK can also upregulate the expression of DNA repair protein poly ADP-ribose polymerase 1 and heat shock protein to delay cellular senescence. This review discusses recent advances in understanding the function of JNK signaling in cellular senescence and includes a comprehensive analysis of the molecular mechanisms underlying JNK-mediated senescence evasion and oncogene-induced cellular senescence. We also summarize the research progress in anti-aging agents that target JNK signaling. This study will contribute to a better understanding of the molecular targets of cellular senescence and provides insights into anti-aging, which may be used to develop drugs for the treatment of aging-related diseases.
MeSH term(s)	Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; Signal Transduction ; Cellular Senescence ; MAP Kinase Signaling System ; Hypoxia
Chemical Substances	JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2023-06-19
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-023-03540-1
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Article ; Online: Esketamine inhibits the c-Jun N-terminal kinase pathway in the spinal dorsal horn to relieve bone cancer pain in rats.

Duan, Chenxia / Zhu, Yi / Zhang, Zhuoliang / Wu, Tiantian / Shen, Mengwei / Xu, Jinfu / Gao, Wenxin / Pan, Jianhua / Wei, Lei / Su, Huibin / Shi, Chenghuan

Molecular pain

2024 Volume 20, Page(s) 17448069241239231

Abstract: ... CXCL12/CXCR4 signals, and c-Jun, as activator protein AP-1 components, contribute to the development ... explored that CXCL12/CXCR4, p-MAPKs, and p-c-Jun were stably up-regulated in the spinal cord ... of CXCL12/CXCR4, p-MAPKs (p-JNK, p-ERK, p-p38 MAPK), and p-c-Jun in microglia. Intrathecal injection ...

Abstract	Cancer-induced bone pain (CIBP) is one of the most common and feared symptoms in patients with advanced tumors. The X-C motif chemokine ligand 12 (CXCL12) and the CXCR4 receptor have been associated with glial cell activation in bone cancer pain. Moreover, mitogen-activated protein kinases (MAPKs), as downstream CXCL12/CXCR4 signals, and c-Jun, as activator protein AP-1 components, contribute to the development of various types of pain. However, the specific CIBP mechanisms remain unknown. Esketamine is a non-selective N-methyl-d-aspartic acid receptor (NMDA) inhibitor commonly used as an analgesic in the clinic, but its analgesic mechanism in bone cancer pain remains unclear. We used a tumor cell implantation (TCI) model and explored that CXCL12/CXCR4, p-MAPKs, and p-c-Jun were stably up-regulated in the spinal cord. Immunofluorescence images showed activated microglia in the spinal cord on day 14 after TCI and co-expression of CXCL12/CXCR4, p-MAPKs (p-JNK, p-ERK, p-p38 MAPK), and p-c-Jun in microglia. Intrathecal injection of the CXCR4 inhibitor AMD3100 reduced JNK and c-Jun phosphorylations, and intrathecal injection of the JNK inhibitor SP600125 and esketamine also alleviated TCI-induced pain and reduced the expression of p-JNK and p-c-Jun in microglia. Overall, our data suggest that the CXCL12/CXCR4-JNK-c-Jun signaling pathway of microglia in the spinal cord mediates neuronal sensitization and pain hypersensitivity in cancer-induced bone pain and that esketamine exerts its analgesic effect by inhibiting the JNK-c-Jun pathway.
MeSH term(s)	Humans ; Rats ; Animals ; Cancer Pain/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Rats, Sprague-Dawley ; Pain/metabolism ; Bone Neoplasms/complications ; Spinal Cord/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Spinal Cord Dorsal Horn/metabolism ; Analgesics/pharmacology ; Hyperalgesia/metabolism ; Ketamine
Chemical Substances	Esketamine (50LFG02TXD) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Analgesics ; Ketamine (690G0D6V8H)
Language	English
Publishing date	2024-02-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2174252-2
ISSN	1744-8069 ; 1744-8069
ISSN (online)	1744-8069
ISSN	1744-8069
DOI	10.1177/17448069241239231
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Article ; Online: S100P facilitates LUAD progression via PKA/c-Jun-mediated tumor-associated macrophage recruitment and polarization.

Gao, Lu / Bai, Ying / Zhou, Jiawei / Liang, Chao / Dong, Yunjia / Han, Tao / Liu, Yafeng / Guo, Jianqiang / Wu, Jing / Hu, Dong

Cellular signalling

2024 , Page(s) 111179

Abstract: ... of chemokines and polarizing factors by activating the PKA/c-Jun pathway, which is implicated in TAM recruitment ... and polarization towards the M2 phenotype. Moreover, inhibition of c-Jun expression impedes ... that S100P facilitates LUAD cells growth by recruiting M2 TAMs through PKA/c-Jun signaling, resulting ...

Abstract	S100P, a member of the S100 calcium-binding protein family, is closely associated with abnormal proliferation, invasion, and metastasis of various cancers. However, its role in the lung adenocarcinoma (LUAD) tumor microenvironment (TME) remains unclear. In this study, we observed specific expression of S100P on tumor cells in LUAD patients through tissue immunofluorescence analysis. Furthermore, this expression was strongly correlated with the recruitment and polarization of tumor-associated macrophages (TAMs). Bioinformatics analysis revealed that high S100P expression is associated with poorer overall survival in LUAD patients. Subsequently, a subcutaneous mouse model demonstrated that S100P promotes recruitment and polarization of TAMs towards the M2 type. Finally, in vitro studies on LUAD cells revealed that S100P enhances the secretion of chemokines and polarizing factors by activating the PKA/c-Jun pathway, which is implicated in TAM recruitment and polarization towards the M2 phenotype. Moreover, inhibition of c-Jun expression impedes the ability of TAMs to infiltrate and polarize towards the M2 phenotype. In conclusion, our study demonstrates that S100P facilitates LUAD cells growth by recruiting M2 TAMs through PKA/c-Jun signaling, resulting in the production of various cytokines. Considering these findings, S100P holds promise as an important diagnostic marker and potential therapeutic target for LUAD.
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2024.111179
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Article ; Online: ZBTB7B is a permissive regulator of hepatocellular carcinoma initiation by repressing c-Jun expression and function.

Zhu, Yue / Wang, Qinqin / Xie, Xinyu / Ma, Cuihong / Qiao, Yuemei / Zhang, Yu / Wu, Yanjun / Gao, Yuan / Jiang, Jing / Liu, Xin / Chen, Jianfeng / Li, Chen / Ge, Gaoxiang

Cell death & disease

2024 Volume 15, Issue 1, Page(s) 55

Abstract: ... Integrative multi-omics analyses identify c-Jun as the core signaling node in ZBTB7B-deficient liver cancer ... initiation. c-Jun is a direct target of ZBTB7B essential to accelerated liver cancer initiation in ZBTB7B ... deficient livers. Knockdown of c-Jun expression or dominant negative c-Jun expression delays HCC development ...

Abstract	Hepatocarcinogenesis is a multi-step process. However, the regulators of hepatocellular carcinoma (HCC) initiation are understudied. Adult liver-specific gene expression was globally downregulated in HCC. We hypothesize that adult liver-specific genes, especially adult liver-enriched transcription factors may exert tumor-suppressive functions in HCC. In this study, we identify ZBTB7B, an adult liver-enriched transcription factor as a permissive regulator of HCC initiation. ZBTB7B is highly expressed in hepatocytes in adult livers, compared to fetal livers. To evaluate the functions of ZBTB7B in hepatocarcinogenesis, we performed hepatocyte-specific ZBTB7B knockout in hydrodynamic oncogene transfer-induced mouse liver cancer models. Hepatocyte-specific knockout of ZBTB7B promotes activated Akt and N-Ras-induced HCC development. Moreover, ZBTB7B deficiency sensitizes hepatocytes to a single oncogene Akt-induced oncogenic transformation and HCC initiation, which is otherwise incompetent in inducing HCC. ZBTB7B deficiency accelerates HCC initiation by down-regulating adult liver-specific gene expression and priming livers to a fetal-like state. The molecular mechanism underlying ZBTB7B functions in hepatocytes was investigated by integrated transcriptomic, phosphoproteomic, and chromatin immunoprecipitation-sequencing analyses. Integrative multi-omics analyses identify c-Jun as the core signaling node in ZBTB7B-deficient liver cancer initiation. c-Jun is a direct target of ZBTB7B essential to accelerated liver cancer initiation in ZBTB7B-deficient livers. Knockdown of c-Jun expression or dominant negative c-Jun expression delays HCC development in ZBTB7B-deficient livers. In addition, ZBTB7B competes with c-Jun for chromatin binding. Ectopic ZBTB7B expression attenuates the tumor-promoting functions of c-Jun. Expression of ZBTB7B signature, composed of 140 genes co-regulated by ZBTB7B and c-Jun, is significantly downregulated in early-stage HCCs compared to adjacent normal tissues, correlates to liver-specific gene expression, and is associated with good prognosis in human HCC. Thus, ZBTB7B functions as a permissive regulator of HCC initiation by directly regulating c-Jun expression and function.
MeSH term(s)	Animals ; Humans ; Mice ; Carcinogenesis/genetics ; Carcinoma, Hepatocellular/pathology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation, Neoplastic ; Liver Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	DNA-Binding Proteins ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Transcription Factors ; Zbtb7b protein, mouse
Language	English
Publishing date	2024-01-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-024-06441-y
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