Ask about this productRelated genes to: TRIM37 Blocking Peptide
- Gene:
- TRIM37 NIH gene
- Name:
- tripartite motif containing 37
- Previous symbol:
- MUL
- Synonyms:
- KIAA0898, POB1, TEF3
- Chromosome:
- 17q22
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-08
- Date modifiied:
- 2016-01-15
Related products to: TRIM37 Blocking Peptide
Related articles to: TRIM37 Blocking Peptide
- Diffuse large B-cell lymphoma (DLBCL) is the most common and clinically aggressive subtype of non-Hodgkin lymphoma, yet key molecular drivers remain incompletely defined. Here, we identify the tripartite motif E3 ligase TRIM37 as a disease-relevant oncogenic factor in DLBCL. TRIM37 was markedly upregulated in patient specimens and cell lines, and high expression correlated with poor prognosis. Loss-of-function studies showed that TRIM37 silencing suppressed proliferation and clonogenicity, triggered apoptosis, and restrained tumor growth in vivo. Mechanistically, TRIM37 promoted ubiquitin-proteasome degradation of the enhancer-associated histone methyltransferase KMT2D, reducing H3K4me1 deposition at the SOCS3 regulatory region, repressing SOCS3, and thereby sustaining JAK2-STAT3 phosphorylation. Rescue experiments supported causality: co-silencing KMT2D or enforcing TRIM37 expression reversed these effects, while JAK2 inhibitor treatment reproduced the impact of TRIM37 loss. Collectively, these findings show that TRIM37 drives DLBCL progression by destabilizing KMT2D to disable SOCS3-mediated negative feedback on JAK2-STAT3 and highlight TRIM37 as a potential therapeutic target. - Source: PubMed
Sun YongchengXiu BingZhou MiaoYang ShujunXu ZhijuanWang ZanzanZhang PingSheng LixiaOuyang GuifangLiang Aibin - The upregulation of the ubiquitin ligase TRIM37 is associated with an adverse prognosis in pancreatic ductal adenocarcinoma (PDAC). This study investigates the mechanism and oncogenic consequence of TRIM37 upregulation in PDAC development. - Source: PubMed
Publication date: 2026/04/01
Yan ChengLi XuanZhao YingChen JinhuiPeng XinkeWu DaichaoChang YabinChen Guodong - Mulibrey nanism is a rare autosomal recessive genetic disorder caused by homozygous or compound heterozygous mutations in the tripartite motif protein 37 ( gene), which codes for a RING finger E3 ubiquitin ligase. Affected individuals present with prenatal-onset growth failure, abnormalities in multiple organs, and heart disorders, including constrictive pericarditis and restrictive cardiomyopathy. - Source: PubMed
Publication date: 2026/03/03
Zodanu Gloria K EZeigler Angela CMudery JordanWolf CharlotteHwang John HKang XuedongSpeirs AmyWang Lee-KaiBiniwale ReshmaSi Ming-SingHalnon NancySatou Gary M Grody Wayne WVan Arsdell Glen SNelson Stanly FTouma Marlin - The tripartite motif (TRIM) protein family functions as a crucial regulator of innate immunity; however, the specific roles of these proteins in crustaceans remain largely uncharacterized. This study characterizes a novel TRIM37 homolog (EsTRIM37) in the Chinese mitten crab, Eriocheir sinensis. Sequence analysis revealed that EsTRIM37 encodes a 936-amino acid protein containing conserved RING, B-box, BBC, and MATH domains. Quantitative real-time PCR showed that EsTRIM37 is constitutively expressed in all examined tissues, with highest abundance in hemocytes, and is significantly upregulated following challenge with Staphylococcus aureus or Vibrio parahaemolyticus. RNA interference (RNAi)-mediated knockdown of EsTRIM37 severely impaired antibacterial defense in vivo, resulting in increased bacterial burdens and significantly reduced host survival rates. Mechanistically, EsTRIM37 silencing inhibited the nuclear translocation of the transcription factors Dorsal and Relish, key components of the Toll and IMD pathways, respectively. Consequently, the expression of multiple downstream antimicrobial peptides (AMPs) was downregulated. These findings collectively demonstrate that EsTRIM37 acts as an essential positive regulator of antibacterial immunity in E. sinensis, enhancing AMPs production and bacterial clearance. - Source: PubMed
Publication date: 2026/03/23
Shen Long-TengZhang MiaoChen Zi-YiWan Zhi-Cheng - m6A and ubiquitination modifications critically drive lung adenocarcinoma (LUAD) progression and are closely linked to cellular context-such as p53 status. Thus, elucidating how these modifications regulate p53's role in LUAD pathogenesis is vital for targeted therapy. - Source: PubMed
Publication date: 2026/03/12
Ji TingZhao TingtingWang ShuniGuo XiaotongWang TingTan HaiWang ShaojinGang MaChen Juan