SPINK1 antibody - N-terminal region (ARP33865_P050)
- Known as:
- SPINK1 (anti-) - N-terminal region (ARP33865_P050)
- Catalog number:
- arp33865_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SPINK1 antibody - N-terminal region (ARP33865_P050)
Related genes to: SPINK1 antibody - N-terminal region (ARP33865_P050)
- Gene:
- SPINK1 NIH gene
- Name:
- serine peptidase inhibitor, Kazal type 1
- Previous symbol:
- -
- Synonyms:
- Spink3, PCTT, PSTI, TATI
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 1988-06-27
- Date modifiied:
- 2015-03-02
Related products to: SPINK1 antibody - N-terminal region (ARP33865_P050)
Related articles to: SPINK1 antibody - N-terminal region (ARP33865_P050)
- B7-H3/CD276 is an emerging immunotherapy target in cancers. However, limited knowledge of B7-H3 signaling and its role in modulating the tumor microenvironment hinders the clinical application of B7-H3-targeting therapy. Here, we report that B7-H3 plays dual roles in regulating myeloid-derived suppressor cells (MDSCs) and cancer-associated fibroblasts (CAFs), thereby promoting tumor progression and therapy resistance, respectively. We comprehensively characterized a non-canonical function of B7-H3 that triggers MAPK signaling in monocytic MDSCs and induces cellular senescence. The senescent monocytic M-MDSCs secreted chemokines to recruit immunosuppressive granulocytic MDSCs. Genetic deletion or pharmacological inhibition of B7-H3/Cd276 reduced Gr-MDSCs and delayed tumor progression. Nevertheless, the secretory factor SPINK1 derived from MDSCs compensatorily activates EGFR/MEK/ERK signaling in CAFs and promotes their extracellular matrix remodeling features, dampening B7-H3-targeting immunotherapy. Combining the B7-H3 monoclonal antibody with the FDA-approved MEK inhibitor trametinib showed durable anti-tumor effects in preclinical models of castration-resistant prostate cancer by fully attenuating immunosuppressive mechanisms. - Source: PubMed
Publication date: 2026/09/18
Shi WeiXu PingGu QianlinFan ZhenLiang XinWang YinZhao YuehuiMeng ChenlingLeo JavierKim Justin JTeng HongqiZhang JieChen FeiyuChen YangNavin Nicholas EZhao Di - - Source: PubMed
Publication date: 2026/09/18
Attila Nagy ZoltánSahin-Tóth Miklós - Hereditary pancreatitis is a rare genetic disorder, usually associated with gain-of-function mutations in the PRSS1 gene. While in the Indian pediatric population, the SPINK1 mutations are more frequently reported, making PRSS1 mutations, particularly the de novo variants, rare. An 11-year-old school-going Indian girl presented with recurrent acute pancreatitis beginning at the age of 5 years. This progressed to chronic pancreatitis by the age of 10 years. Metabolic, autoimmune, structural, and infectious causes were excluded. The genetic test done revealed a heterozygous pathogenic PRSS1 c.86A>T (p.Asn29Ile) variant. In the absence of family history, this was consistent with a likely de novo mutation. No pathogenic variants were detected in SPINK1, CFTR, CTRC, or CPA1. Pancreatic enzyme replacement therapy and dietary modification reduced the frequency of attacks and preserved her growth. This case highlights the importance of genetic evaluation in children who present with unexplained recurrent pancreatitis, even when there is no positive family history. Early identification of PRSS1 mutation allows for appropriate counseling, long-term surveillance, and complication prevention. - Source: PubMed
Publication date: 2026/09/15
Pande VineetaUpadhyaya Nidhi NReddy Bharath SinhaNepram Amrita - Aberrant expression of mitochondrial quality regulation genes (MQRGs) is intricately linked to mitochondrial dysfunction and the progression of hepatocellular carcinoma (HCC), highlighting the urgent need for reliable prognostic biomarkers. In this study, we aimed to identify differentially expressed MQRGs from 20 candidate genes by analyzing transcriptomic profiles and clinical records from the TCGA (n = 371) and GEO (n = 167) datasets. The identified prognostic MQRGs, along with associated subtype differentially expressed genes (DEGs, n = 156), underwent LASSO and multivariate Cox regression analyses to construct a risk model, which was subsequently validated through time-dependent ROC analysis, Kaplan-Meier curves, and in vitro RT-qPCR. Our findings established a robust 4-MQRG signature comprising ANXA10, BAMBI, AKR1B15, and SPINK1, which revealed that patients classified as high risk had significantly shorter overall survival compared to their low-risk counterparts (p < 0.001). The predictive accuracy of this signature was noteworthy, yielding 1-, 3-, and 5-year AUCs of 0.725, 0.696, and 0.747 in the training cohort (n = 243) and 0.676, 0.627, and 0.592 in the testing cohort (n = 242), respectively. Furthermore, high-risk scores were associated with distinct immunosuppressive tumor microenvironments and varying sensitivity to systemic therapies. The dysregulated expression of the four genes was corroborated by RT-qPCR and analysis of the HPA database. In conclusion, this validated MQRG-based prognostic signature serves as an accurate tool for survival prediction and risk stratification, thus offering valuable biomarker support for personalized therapeutic approaches in HCC. - Source: PubMed
Li BinbinZeng LijunHe ZhilongLuo LunqiLuo YongmeiYi XinyuLi ZhiminZhu HongboLi Yuehua - Glioblastoma (GBM) is the most aggressive and lethal primary brain tumor, and elucidating the molecular determinants of its malignant progression is essential for improving patient outcomes. NTAN1 encodes N-terminal asparagine amidase 1, a component of the N-degron pathway involved in selective protein turnover; however, its role in GBM remains unclear. This study aimed to investigate the clinical significance and biological function of NTAN1 in GBM. Integrated analyses of The Cancer Genome Atlas (TCGA) transcriptomic and clinical data were performed, together with tissue microarray validation, to assess the association between NTAN1 expression and prognosis in GBM. Immunohistochemical analysis of GBM specimens was conducted to evaluate NTAN1 protein expression. Functional studies, including NTAN1 knockdown and overexpression experiments, were used to examine its effects on GBM cell proliferation, clonogenic growth, migration, and invasion. An orthotopic GBM model was established to assess the effect of NTAN1 inhibition on tumor growth. Transcriptomic analysis was further performed to explore the molecular changes associated with NTAN1 knockdown. Elevated NTAN1 expression was associated with poor survival in GBM. Immunohistochemical analysis further demonstrated that high NTAN1 protein expression predicted unfavorable prognosis. Functional studies showed that NTAN1 knockdown inhibited GBM cell proliferation, clonogenic growth, migration, and invasion, whereas NTAN1 overexpression promoted these malignant phenotypes. In an orthotopic GBM model, NTAN1 inhibition significantly reduced tumor volume. Transcriptomic analysis showed that NTAN1 knockdown was associated with reduced expression of invasion-related genes, including , , and , and with enrichment changes in inflammation-associated pathways, suggesting that NTAN1 may promote GBM progression through pro-invasive molecular programs. Collectively, these findings identify NTAN1 as a potential promoter of GBM malignant progression and a prognostic biomarker of poor outcome. - Source: PubMed
Publication date: 2026/08/21
Yang JianLin ZihanWang ZhihanLin ShukaiChen MingleiXu HaoLv QiGao LiGe Jianwei