HCLS1 antibody - N-terminal region (ARP31928_T100)
- Known as:
- HCLS1 (anti-) - N-terminal region (ARP31928_T100)
- Catalog number:
- arp31928_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HCLS1 antibody - N-terminal region (ARP31928_T100)
Related genes to: HCLS1 antibody - N-terminal region (ARP31928_T100)
- Gene:
- HCLS1 NIH gene
- Name:
- hematopoietic cell-specific Lyn substrate 1
- Previous symbol:
- -
- Synonyms:
- HS1, CTTNL
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-26
- Date modifiied:
- 2016-10-05
Related products to: HCLS1 antibody - N-terminal region (ARP31928_T100)
Related articles to: HCLS1 antibody - N-terminal region (ARP31928_T100)
- 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 - Newborns' intestinal adhesions have been reported in 4.7% infants who underwent a laparotomy, but adhesions can also appear idiopathically. Etiology and pathogenesis of adhesions is still to be determined, but evidence shows relation to inflammation, formation of fibrin bands, hypoxia and tissue remodelation. Multiple candidate genes have been associated with adhesion development. The aim of this study was to evaluate the appearance of Sonic Hedgehog (SHH), Indian Hedgehog (IHH), Forkhead-box F1 (FOXF1), caudal type homeobox 1 (CDX1), HCLS1-associated protein X-1 (HAX-1), GATA Binding Protein 4 (GATA4) and Granzyme-B (GZMB) proteins in infant adhesions and to describe possible interfactorial correlations. Adhesion affected tissue samples were collected from 14 patients under one year of age that underwent abdominal surgery to treat partial or complete intestinal obstruction. The control group consisted of 6 individuals that had surgical repairment of inguinal hernia. Routine staining and immunohistochemistry were performed. Immunopositive fibroblasts, macrophages, endotheliocytes, smooth muscle myocytes of blood vessel wall and mesotheliocytes were investigated. The relative distribution of all factors was evaluated by the semiquantitative counting method. Statistical analysis was done using non-parametric tests and correlations were calculated based on Spearman's correlation analysis. A statistically significant decrease was observed for SHH, IHH, FOXF1, GATA4 and partially for GZMB in the adhesion group. There were also decreased HAX-1 and CDX1 immunopositive structures in the adhesion group, however, without any statistical significance. SHH, IHH, FOXF1, GATA4 and GZMB might have a role in adhesion development among infant patients which could suggest a dysregulation of cellular events. Abundance of correlations between the gene protein appearances in different structures indicate the affected blood vessels, fibroblasts and macrophages, however, mesothelium seems not to be the key driver in the morphopathogenesis of adhesion development. - Source: PubMed
Publication date: 2026/02/10
Pauliņš ArvisJunga AnnaPilmane Māra - Lymphoid cancers of different types and subtypes are known to cluster in families. We hypothesize that there are shared susceptibility factors in families with these heterogenous lymphoid malignancies. Exome sequencing was performed on 100 individuals from 43 lymphoid cancer pedigrees. Variants from 37 families were ranked using the eights-based vriant anking in edigrees (WARP) pipeline. Six affected unrelated probands were used for interpretation only. We detected recurrent variants in the germline lymphoid cancer gene in 4 (9%) of the 43 families, and variants in other genes involved in lymphoid cancers: and . Variants in genes including and involved in the WNT/β-catenin pathway were identified, representing a novel observation. Some variants appeared to segregate with specific types of lymphoid cancers; others were shared across different subtypes. Identifying factors predisposing to different types of lymphoid cancers will help understand the etiology of these neoplasms. - Source: PubMed
Publication date: 2026/02/07
Ralli SnehaJones Samantha JeanLeach StephenLynch Henry JBrooks-Wilson Angela R - Ulcerative colitis (UC) is an immune-mediated chronic inflammatory bowel disease, and with the rising global incidence and the risk of malignant transformation, the treatment of UC is challenged by heterogeneous progression and limited targeted therapies, and its underlying pathogenesis remains unclear. This study aims to identify novel therapeutic targets for UC, elucidate the genetic factors associated with UC development, and advance precision medicine strategies for UC. - Source: PubMed
Publication date: 2025/12/08
Zhu XiangYang YujieZhu Yi - Casitas B lymphoma-b (Cbl-b) is an E3 ubiquitin ligase that serves as a critical brake on immune cell activations. It negatively fine-tunes immune responses through ubiquitination of signaling proteins. Cbl-b deficiency in mice leads to spontaneous tumor rejection and induces only mild, non-lethal autoimmunity, highlighting its potential as a promising immunotherapy target. NX-1607 is the first oral small molecule inhibitor of Cbl-b and it is currently in phase I clinical trial. A recent publication employed high-throughput drug combination screening to systematically elucidate the molecular pathways by which NX-1607 enhances T cell activation. The authors administered 81 well-characterized inhibitors to Jurkat T cells under CD3-stimulated and unstimulated conditions in the presence of NX-1607. Inhibitors of the MAPK/ERK pathway significantly attenuated NX-1607-enhanced T cell activation as indicated by CD69 markers. Proto-oncogene tyrosine-protein kinase Src (SRC) family kinase inhibitors also reduced both CD69 activation markers and the phosphorylation of PLCγ1 and HCLS1 which are upstream of MAPK/ERK pathways. These findings were validated in an immunocompetent B-cell lymphoma mouse model, where NX-1607 consistently upregulated PLCγ1 and ERK phosphorylation. Together, this work delineates a PLCγ1-MAPK/ERK axis through which Cbl-b inhibition unleashes T cell activation, providing critical insight for the development of NX-1607 based immunotherapy. - Source: PubMed
Publication date: 2025/12/25
To AlexSugimura Ryohichi