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
- 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 - Increasing evidences indicate that unlimited capacity for self-renewal and pluripotency, two unique properties of embryonic stem cells (ESCs), are intrinsically linked to cell cycle control. However, the precise mechanisms coordinating cell fate decisions and cell cycle regulation remain to be fully explored. Here, using CRISPR/Cas9-mediated genome editing, we show that in ESCs, deficiency of components of the cell cycle regulatory MuvB complex Lin54 or Lin52, but not Lin9 or Lin37, triggers G2/M arrest, loss of pluripotency, and spontaneous differentiation. Further dissection of these phenotypes demonstrated that this cell cycle arrest is accompanied by the gradual activation of mesoendodermal lineage-specifying genes. Strikingly, the abnormalities observed in Lin54-null ESCs were partially but significantly rescued by ectopic coexpression of genes encoding G2/M proteins Cyclin B1 and Cdk1. Thus, our study provides new insights into the mechanisms by which the MuvB complex determines cell fate through regulation of the cell cycle machinery. - Source: PubMed
Publication date: 2022/02/09
Wang CongcongHao KunyingDong LixiaWang JingnanZhao LinchunXu LijunXia YinJiang QingQin Jinzhong