TRIM24 antibody - middle region (ARP34449_P050)
- Known as:
- TRIM24 (anti-) - middle region (ARP34449_P050)
- Catalog number:
- arp34449_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TRIM24 antibody - middle region (ARP34449_P050)
Related genes to: TRIM24 antibody - middle region (ARP34449_P050)
- Gene:
- TRIM24 NIH gene
- Name:
- tripartite motif containing 24
- Previous symbol:
- TIF1
- Synonyms:
- hTIF1, Tif1a, RNF82, TIF1A
- Chromosome:
- 7q33-q34
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-18
- Date modifiied:
- 2018-02-13
Related products to: TRIM24 antibody - middle region (ARP34449_P050)
Related articles to: TRIM24 antibody - middle region (ARP34449_P050)
- Histone deacetylases (HDACs) play critical roles in immune regulation and inflammatory responses in sepsis. This study identified HDAC-related genes and explored their potential roles in sepsis. - Source: PubMed
Publication date: 2026/04/06
Wang YuanyuanShu TaoLi YanpengKang QiangqiangJia ZhanshengMa Chunyan - Oncogenic RET gene rearrangements drive a subset of lung adenocarcinomas (LUAD) and the tyrosine kinase inhibitors (TKIs) selpercatinib and pralsetinib are approved therapeutics. However, acquired resistance remains a hurdle to durable management. Two RET+ lung cancer cell lines (TR.1, TR.2) were established from a Trim24-Ret mouse model and lung tumors resulting from their orthotopic transplantation initially responded to selpercatinib followed by prompt progression within ∼3 weeks of initiating TKI treatment. Cell lines derived from the selpercatinib-resistant TR.1 and TR.2 tumors exhibited in vitro sensitivity to MET and ERBB-targeted TKIs, indicating acquired bypass signaling through these receptor tyrosine kinases (RTKs). The TKI-resistant cell lines showed no evidence for MET gene amplification, but exhibited transcriptional induction of genes that function within MET and ERBB2:ERBB4 interaction networks including ligands (HGF, NRG1), adaptors (GAB1) and co-receptors (NRP1). Exogenous HGF, but not NRG1 reversed in vitro growth inhibition by selpercatinib in TR.1 and TR.2 cells. Mice bearing orthotopic TR.1 or TR.2 lung tumors progressing on selpercatinib underwent significant re-shrinkage upon co-treatment with the MET inhibitor, crizotinib, although similar to the clinical experience, progression again occurred. By contrast, upfront treatment with selpercatinib and crizotinib in orthotopic tumors yielded complete elimination of 7 of 9 TR.1 tumors and both deepened and prolonged the duration of response in TR.2 tumors. The findings provide new insight into mechanisms of acquired resistance through bypass signaling and highlight the therapeutic benefit of simultaneous upfront blockade of driver oncogenes and dominant resistance mechanisms in LUAD. - Source: PubMed
Publication date: 2026/03/30
Hinz Trista KLe Anh TDoan TristanAst AbbyJaramillo SophiaAvila Jasalyn TSkhisov DanielHaines SamanthaNavarro Andre CPatil TejasNemenoff Raphael AHeasley Lynn E - The turnaround of the tumor suppressor p53 protein, the guardian of the genome, is closely regulated to ensure avoidance of its untimely activation, which could lead to the demise of normal cells. Cancer cells often display mutations in the gene encoding for p53, which interferes with its normal function. The genomic series of colorectal cancer from the Cancer Genome Atlas (TCGA) was interrogated to discover genomic alterations and determine the mRNA expression of enzymes affecting p53 ubiquitination in colorectal cancers with wild-type and mutant . Genomic alterations of p53-regulating E3 ubiquitin ligases were uncommon in colorectal cancers, the most frequent being mutations in . Several p53-regulating E3 ligases were well expressed in subsets of colorectal cancers, two of which, MDM2 and TRIM24, displayed higher mRNA expressions than the normal colorectal epithelia. The former was particularly upregulated in wild-type colorectal cancers, and the latter was upregulated in both wild-type and mutant cancers. Upregulation of TRIM24 in mutant cancers was observed independently of the type of mutations (gain-of-function or other). Among E3 ligases used in proteolysis-targeting chimeras (PROTACs), VHL was upregulated together with its E2-conjugating enzyme UBE2S in colorectal cancers. This survey of p53-targeting ubiquitin ligases provides a roadmap for potential therapeutic strategies working by promoting the destruction of the mutant protein or reactivating its normal function in -mutated colorectal cancers and promoting p53 function by preventing degradation in wild-type cancers. - Source: PubMed
Publication date: 2026/02/26
Voutsadakis Ioannis A - fusion-positive NSCLC is driven by a range of fusion partners, most often . The clinical impact, oncogenicity, and resistance mechanisms of rare, noncanonical fusions remain underexplored. We describe two previously unreported fusion partners in NSCLC and explore the potential mechanisms of resistance in each case, including on-target and bypass mutations, as well as the use of next-generation sequencing (NGS) testing on cerebrospinal fluid (CSF) as a useful tool. - Source: PubMed
Publication date: 2025/11/21
Hsu CharlesYakoub MohamedOffin MichaelEng JulianaDrilon AlexanderYang Soo-Ryum - Around 30% of patients with hormone receptor-positive (HR+) breast cancer acquire resistance to endocrine therapy combined with cyclin-dependent kinase 4/6 inhibitors (CDK4/6i), which are first-line treatments in metastatic settings. Therefore, we aimed to identify loci associated with resistance to endocrine therapy and CDK4/6i; this was achieved using retroviral vectors, which randomly insert gene-disrupting elements into the genome, causing gene expression alterations and potentially leading to therapy resistance. ER-positive ZR75.1 breast cancer cells transduced with retroviral vectors were treated with endocrine (tamoxifen, fulvestrant) or CDK4/6i monotherapies (abemaciclib, palbociclib, ribociclib) or a combination of fulvestrant and ribociclib. DNA was extracted, and virus integration sites (VISs) were characterized according to the detection frequency and read depth using next-generation sequencing (VIS-NGS). Resistance-associated VIS loci were identified when differentially presented in treated samples compared to controls. Well-established tamoxifen resistance genes (, , ) were detected, enabling the validation of our approach. Thirty-seven VIS loci were associated with resistance to fulvestrant and ribociclib monotherapies. Twenty of these loci were also identified as candidates for resistance to other CDK4/6i and to fulvestrant and ribociclib combination therapy, including and -genes that are involved in resistance to endocrine therapy but have not yet been associated with resistance to CDK4/6i. The identification of unique and shared resistance-associated loci highlights the complexity of resistance pathways. - Source: PubMed
Publication date: 2026/01/29
Huang ZhangzanBeaufort CorineHelmijr JeanZantboer BrianRozema GiadaMuritti CamillaWhien Julia JUijterwegen AnnaMassimino MicheleMartens John W MJansen Maurice P H M