Ask about this productRelated genes to: HS1BP3 antibody
- Gene:
- HS1BP3 NIH gene
- Name:
- HCLS1 binding protein 3
- Previous symbol:
- -
- Synonyms:
- HS1-BP3,FLJ14249
- Chromosome:
- 2p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-15
- Date modifiied:
- 2014-11-19
Related products to: HS1BP3 antibody
Related articles to: HS1BP3 antibody
- The HCLS1-Binding Protein 3 (HS1BP3) interacts with the SH3 domain of cortactin (CTTN), a protein that contributes to a malignant phenotype in cancers. Here, we demonstrate that high expression of HS1BP3 is associated with reduced survival for gastric adenocarcinoma and triple negative breast carcinoma patients and that HS1BP3 is specifically upregulated in these cancers. We mapped the HS1BP3-cortactin interaction site to the third proline-rich region (PRR3.1) of HS1BP3 and show that this interaction is important for cancer cell proliferation, extracellular matrix degradation and secretion. HS1BP3 expression was found to correlate with expression of the invadopodia scaffold protein TKS5 and we show that the localisation of TKS5 inside multivesicular endosomes is increased in cells expressing an HS1BP3 PRR3.1 mutant. Overall, our results highlight the importance of the direct interaction between HS1BP3 and cortactin in cancer development by regulating cell proliferation, secretion and invasion, which may provide an explanation for the negative correlation between HS1BP3 levels and the survival of gastric adenocarcinoma and triple negative breast cancer patients. - Source: PubMed
Publication date: 2026/04/10
Løchen Arja ArnesenSøreng KristianeVeroni ChiaraTrachsel-Moncho LauraAsp NaghamGaupset RobinLyckander Lars GustavKnævelsrud HeleneEftang LarsSimonsen Anne - Chemoradiation prior to surgery in locally advanced rectal cancer is the current standard therapy but is not effective in all rectal cancer patients. Prognostic markers supporting patient stratification with respect to clinical response would therefore be desirable. The aim of this study was to investigate pathophysiological mechanisms underlying radioresistance and to identify potential prognostic markers by comparative proteome profiling. Therefore, formalin fixed paraffin-embedded tissue (FFPE) samples from rectal tumors ( = 50) and normal control tissue ( = 39) of nonresponders and responders to neoadjuvant chemoradiation were analyzed. As a result, 1685 robustly identified proteins were further evaluated. Comparing tumor with corresponding control samples revealed 221 differentially expressed proteins (FDR < 0.05) with FTL, PCOLCE, and RCN3 being most striking in tumor tissue. CEACAM 1, 5, and 6, as well as MCM protein complex components, were significantly up-regulated in tumor tissue of nonresponders. The autophagic activity-related and DNA damage repair proteins TOM1, CAPNS1, TP53BP1, HS1BP3, as well as COTL1 and DCPS, discriminated non- and nearly complete from complete responders. In the tumor-surrounding tissue of nonresponders, the innate immune response-suppressing protein CD55 was found specifically up-regulated. These proteins may serve as prognostic markers and potential therapeutic targets, requiring further validation in prospective studies. - Source: PubMed
Publication date: 2025/06/26
Zott TobiasWolf MichaelPlessl-Walder GünterRegele HeinzBergmann MichaelMeier-Menches Samuel MGerner ChristopherSilberhumer Gerd RBileck Andrea - This study combines two innovative mouse models in a major gene discovery project to assess the influence of host genetics on asbestos related disease (ARD). Conventional genetics studies provided evidence that some susceptibility to mesothelioma is genetic. However, the identification of host modifier genes, the roles they may play, and whether they contribute to disease susceptibility remain unknown. Here we report a study designed to rapidly identify genes associated with mesothelioma susceptibility by combining the Collaborative Cross (CC) resource with the well-characterised MexTAg mesothelioma mouse model. The CC is a powerful mouse resource that harnesses over 90% of common genetic variation in the mouse species, allowing rapid identification of genes mediating complex traits. MexTAg mice rapidly, uniformly, and predictably develop mesothelioma, but only after asbestos exposure. To assess the influence of host genetics on ARD, we crossed 72 genetically distinct CC mouse strains with MexTAg mice and exposed the resulting CC-MexTAg (CCMT) progeny to asbestos and monitored them for traits including overall survival, the time to ARD onset (latency), the time between ARD onset and euthanasia (disease progression) and ascites volume. We identified phenotype-specific modifier genes associated with these traits and we validated the role of human orthologues in asbestos-induced carcinogenesis using human mesothelioma datasets. We generated 72 genetically distinct CCMT strains and exposed their progeny (2,562 in total) to asbestos. Reflecting the genetic diversity of the CC, there was considerable variation in overall survival and disease latency. Surprisingly, however, there was no variation in disease progression, demonstrating that host genetic factors do have a significant influence during disease latency but have a limited role once disease is established. Quantitative trait loci (QTL) affecting ARD survival/latency were identified on chromosomes 6, 12 and X. Of the 97-protein coding candidate modifier genes that spanned these QTL, eight genes ( and ) were found to significantly affect outcome in both CCMT and human mesothelioma datasets. Host genetic factors affect susceptibility to development of asbestos associated disease. However, following mesothelioma establishment, genetic variation in molecular or immunological mechanisms did not affect disease progression. Identification of multiple candidate modifier genes and their human homologues with known associations in other advanced stage or metastatic cancers highlights the complexity of ARD and may provide a pathway to identify novel therapeutic targets. - Source: PubMed
Publication date: 2024/04/17
Fisher Scott APatrick KimberleyHoang TracyMarcq EllyBehrouzfar KiarashYoung SylviaMiller Timothy JRobinson Bruce W SBueno RaphaelNowak Anna KLesterhuis W JoostMorahan GrantLake Richard A - To explore the role of HS1-binding protein 3 (HS1BP3) in hepatocellular carcinoma (HCC) and the potential mechanism. - Source: PubMed
Publication date: 2022/07/19
Hu XiaosiPan HongtaoZhou ShuaiPang QingWang YongZhu ChaoLiu HuichunJin HaoXu Aman - Alzheimer's disease (AD) is a neurodegenerative disease that is characterized by a devastating decline in cognitive activities among all types of dementia, and it severely affects the quality of life. Late-onset AD (LOAD) occurs after the age of 65 years and develops sporadically. Although aging comes first along the main risk factors underlying LOAD, disease-causing susceptibility genes have been associated with disease pathogenesis. In our study, we included the genes , , , , , and to be investigated in LOAD patients based on their expression levels. Within this framework, we aimed to determine the possible functions of these genes in the pathophysiology of the disease. We investigated whether the utilization of these genes as biomarkers in the early diagnosis of LOAD may help the treatment scheme to be applied in the clinic. We involved 50 individuals in the study and collected peripheral blood samples from the patients and control groups for molecular genetic analysis. Subsequently, RNA was extracted from the peripheral blood samples, and expression analyzes were performed using qualitative reverse transcription polymerase chain reaction. The results obtained were evaluated by using proper statistical methods. Our results demonstrated that there was no difference between patient and control groups in terms of , , , and genes. The expression levels of the and genes were significantly lower in the patient group compared with the control group. In conclusion, we presume that the and genes can be utilized as molecular biomarkers for LOAD. - Source: PubMed
Publication date: 2022/03/08
Kenanoglu SercanKandemir NefiseAkalin HilalGokce NuriyeGol Mehmet FGultekin MuratKoseoglu EmelMirza MeralDundar Munis