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)
- 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 - Consensus molecular classes of urothelial carcinoma (UC) include basal/squamous (Ba/Sq), luminal papillary (LumP), luminal nonspecified (LumNS), luminal unstable (LumU), stroma-rich, and neuroendocrine (NE)-like. We aimed to determine the consensus molecular classifications of micropapillary (MP), plasmacytoid (PC), and sarcomatoid (SM) subtypes of bladder UC and characterize their spatial transcriptomic profiles. - Source: PubMed
Publication date: 2026/08/25
Zhao TingNawrocki ColeXiong LinjieNieman Linda TSaylor Philip JBlute Michael LMiyamoto David TTing David TDahl Douglas MWu Chin-Lee - Pancreatic ductal adenocarcinoma (PDAC) is a devastating cancer with increasing incidence and a dismal prognosis. Here, we uncover serine protease inhibitor Kazal type 1 (SPINK1) as a putative determinant of PDAC progression with a previously unrecognized role in epigenomic regulation. We show that SPINK1 expression, which is highly dynamic across PDAC progression, is associated with key aggressive cancer phenotypic states and regulates cancer cell stemness and plasticity in both in vitro and patient samples. Mechanistically, our results suggest a new signaling axis where SPINK1 interacts with COL18A1 to promote its cleavage into endostatin, which then induces histone H3 modifications. These results reveal a new function of SPINK1 in PDAC and highlight the SPINK1-COL18A1-endostatin signaling axis as a potential therapeutic target to combat PDAC aggressiveness. - Source: PubMed
Publication date: 2026/08/18
Tang HaoyuSailo BethsebieShang XingboHossan Md ShahadatKratz JeremyDas ParomitaChhoda AnkitAldo PaulomiLiu HeRobert Marie EDoucette SarynParis Timothy JKunstman John WPappou EmmanouilWood Laura DIacobuzio-Donahue Christine AWolfgang Christopher LMazzetto MariateresaHe LindaPfaff MarieAng-Olson OliviaHoggard TimothyGarcia-Milian RolandoSharma AnupLevchenko AndreAhuja Nita - Inflammatory bowel disease (IBD) is a systemic disorder that affects not only the gastrointestinal tract but also extraintestinal organs and is associated with a significantly increased risk of osteoporosis. This study aims to investigate the association between plasma proteomic profiles and the subsequent risk of osteoporosis in patients with IBD. - Source: PubMed
Publication date: 2026/08/04
Yue MinYe XiaohuaJin ZhenheYe KexinXu ChengweiZhou TianyuShen Zhe - This study aimed to investigate the associations between SNPs in , , and genes and the clinical characteristics of refractory FD including clinical symptoms, pancreatic enzyme abnormalities, and exocrine pancreatic function. - Source: PubMed
Publication date: 2026/08/10
Nakamura KenFutagami SeijiHigashida SakuraAgawa ShuheiKawawa RieHabiro MayuKirita KumikoOnda TakeshiTanabe TomohideUeki NobueHonda KazufumiGwee Kok-AnnIwakiri KatsuhikoAtsukawa Masanori