Ask about this productRelated genes to: LIN37 antibody
- Gene:
- LIN37 NIH gene
- Name:
- lin-37 DREAM MuvB core complex component
- Previous symbol:
- -
- Synonyms:
- ZK418.4, F25965, lin-37
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2007-05-17
- Date modifiied:
- 2014-07-17
Related products to: LIN37 antibody
Related articles to: LIN37 antibody
- Tyrosine kinase inhibitor (TKI) resistance severely limits clinical outcomes in hepatocellular carcinoma (HCC), highlighting the urgent need to elucidate its underlying molecular mechanisms. In this study, an unbiased genome-wide CRISPR/Cas9 screening identified novel key factors related to the therapeutic responsiveness of TKI in HCC. By integrating data from 20 datasets encompassing 322 samples, a comprehensive TKI therapeutic response landscape for HCC was constructed. GO and Reactome enrichment analyses revealed that dysregulated RNA splicing, ubiquitination, endocytosis/exocytosis, and cell cycle pathways modulate TKI sensitivity, with close links to antitumor immunity. This study identified GPATCH4, CCT3, C19orf53, UACA, PPM1M, and LIN37 as key genes mediating TKI resistance in HCC. These six genes were found to be highly expressed in HCC and significantly associated with HCC patient prognosis. Drug sensitivity assays identified a significant association between their expression and responsiveness to TKI agents. In-house quantitative real-time PCR validated their differential expression levels in normal hepatocytes, parental HCC cells, and TKI-resistant HCC sublines. ssGSEA, TIMER2, and ESTIMATE analysis revealed that their expression modulates HCC immune infiltration. Bibliometric analysis revealed a growing focus on immunotherapy-based combination regimens to overcome TKI resistance. Ferroptosis, epithelial-mesenchymal transition and hypoxia were new research directions, which were closely related to the pathways investigated in this study. In conclusion, this study identified RNA splicing, ubiquitination, endocytosis/exocytosis, and cell cycle pathways, as well as GPATCH4, CCT3, C19orf53, UACA, PPM1M, and LIN37, as novel directions and targets for TKI-immunotherapy combination strategies, providing new insights for overcoming TKI resistance in HCC. - Source: PubMed
Chen Si-YuYang Li-HuaLiang Zi-QianLi Jian-DiLi Shi-deDeng Yu-LongChen Guo-QiangLing Jing-WenZhou Sheng-ShengChen GangHe Rong-Quan - Poorly differentiated endometrial carcinoma in Black African women is under-characterized at the transcriptomic level, although it is known for aggressive subtypes. We conducted the first RNA-seq analysis of formalin-fixed, paraffin-embedded (FFPE) tumors from Black South African women to explore population-specific gene expression, alternative splicing, and novel isoforms. - Source: PubMed
Publication date: 2026/03/24
Molefi ThuloAlaouna MohammedChipiti TalentSebitloane HannahDlamini Zodwa - (p107) is a member of the retinoblastoma (RB) family of pocket proteins involved in cell cycle regulation and E2F transcriptional repression. While its promoter contains conserved E2F motifs, the integrated regulation of by upstream tumor suppressor pathways remains incompletely understood. Here, we investigate the p53-dependent transcriptional regulation of and dissect the contribution of its tandem E2F binding sites to this mechanism. Luciferase assays in synchronized cells demonstrated that these two conserved E2F sites are required for cell cycle-dependent activation of the promoter. Overexpression of p53 showed that p53 represses promoter activity in an E2F site-dependent manner. Using HCT116 p21 knockout cells, we revealed that this p53-dependent repression is mediated by p21. Chromatin immunoprecipitation confirmed dynamic in vivo binding of E2F1-3 and E2F4, while DNA pull-down assays revealed specific in vitro recruitment of RB, p107, and E2F1-4 to the two E2F sites, along with weak binding of MuvB components. Additional experiments in RB and LIN37 knockouts showed that RB/E2F repressing complex plays the main role in repressing the promoter, while E2F4, p107, and p130 can support this effect to a lesser extent. Overall, our findings demonstrate that p53 controls expression indirectly through the p21-RB-E2F pathway by utilizing two E2F binding sites within the promoter. - Source: PubMed
Publication date: 2025/10/11
Azzahrani KhaledAlqahtani Faleh - As modest increases in temperature become more common due to global climate change, organisms are being subjected to moderate temperature stresses that can disproportionally affect fertility. Species that can buffer fluctuations in temperature through tissue or cellular responses in the germ line will therefore be more likely to survive moderate temperature stresses. Currently, what mechanisms are used in the germ line to facilitate maintenance of fertility under moderate temperature stress remain unknown. To address this, we investigated how germline apoptosis is modulated in Caenorhabditis elegans nematodes in response to moderate temperature stress. We found that wild-type animals increase their germline apoptosis levels from the physiological baseline in response to the moderate temperature stress. This induction of germline apoptosis was dependent on known and novel regulators of germline apoptosis including members of the conserved DREAM (Dp, Retinoblastoma (Rb)-like, E2F, MuvB) complex: LIN-35/pRB, LIN-54, and LIN-37, and proteins that regulate the synapsis checkpoint, BUB-3 and PCH-2. Additionally, repression of CED-9 function, the C. elegans Bcl2 ortholog, was necessary for full induction of apoptosis during moderate temperature stress. Finally, we found that changes in cytoplasmic streaming are correlated with changes to oocyte provisioning in wild-type animals but not mutants. Together, these data suggest an expanded role for LIN-35, the MuvB core of the DREAM complex, CED-9, and the synapsis checkpoint in maintaining fertility by activating apoptosis during moderate temperature stress. - Source: PubMed
Compere Frances VQuaglia Kristen ACrespo Cruz Margaret NLorenzen Hannah NOswald Samantha HUttal KatherinePetrella Lisa N - The deregulated expression of the c-MYC oncogene activates p53, which is presumably mediated by ARF/INK4, as well as replication-stress-induced DNA damage. Here, we aimed to determine whether the c-MYC-inducible AP4 transcription factor plays a role in this context using a genetic approach. - Source: PubMed
Publication date: 2023/02/11
Kaller MarkusShi WenjingHermeking Heiko