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)
Ask about this productRelated 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)
- We report a multicystic intrahepatic neoplasm in a 54-year-old Japanese woman, representing a previously unrecognized subtype. Grossly, the lesion was a well-demarcated multicystic tumor with focal papillary projections. Histologically, the cysts were lined by columnar to cuboidal neoplastic cells with brush border-like luminal microvilli, abundant granular eosinophilic cytoplasm, and small round nuclei. The cystic lumina contained colloid-like secretion, and bile-filled glands were occasionally observed. The septa were composed of thin hepatocellular parenchyma. Immunohistochemically, the tumor cells were positive for CD10, CK7, CK19, EpCAM, and SPINK1 and negative for HepPar1, MUC1, MUC2, MUC5AC, and MUC6. Whole-exome sequencing identified a pathogenic somatic KRAS p.G12V variant. RNA sequencing detected no PRKACA/B fusions. Single-cell spatial transcriptomics demonstrated that tumor cells clustered most closely with septal and medium-sized interlobular bile ducts. Gene set activity analysis showed significant suppression of gene sets downregulated by KRAS activation and upregulation of KRAS dependency signature gene sets in tumor cells. These findings distinguish this lesion from established entities of intrahepatic biliary cystic neoplasms, including intraductal papillary neoplasm, intraductal tubulopapillary neoplasm, intraductal oncocytic papillary neoplasm, and mucinous cystic neoplasm. We propose the designation "eosinophilic biliary cystic neoplasm of the liver" for this distinct intrahepatic biliary neoplasm. - Source: PubMed
Tanaka MarikoKoinuma DaizoHinata MunetoshiTakeshita KimikoYasunaga YoichiSakuma KeiTakamoto TakeshiNishioka YujiroHasegawa KiyoshiNakai YudaiUshiku Tetsuo - A trypsin inhibitor, the serine peptidase inhibitor, Kazal type 1 (SPINK1), a secreted protein, has been identified in recent years as contributing to the advancement of specific cancer types. Lung cancer is a common class of malignant tumors. However, the role of SPINK1 in lung cancer is unknown. This study aimed to investigate the profound mechanism of SPINK1 in lung cancer. - Source: PubMed
Publication date: 2026/03/19
Yue GuojunYue LingyunChen YanYang HengChen XiZhao YaqianXing ShiyunShen GangZhou LeiZhang YuBai Yiju - - Source: PubMed
Publication date: 2026/04/01
Berke GergőAbu-El-Haija MaisamMorgan KatherineSingh Vikesh KBellin Melena DSahin-Tóth Miklós - Variants with intermediate functional effects-neither fully disruptive nor functionally neutral-represent an underrecognized source of genetic complexity and define a functional grey zone that complicates variant classification. Here, we address this issue using GT>GC (+2T>C) 5' splice-site variants as a tractable model, as approximately 15-18% of such substitutions retain variable levels of residual wild-type (WT) transcript. Using residual WT transcript as a quantitative functional readout, we first revisited disease-associated GT>GC variants previously shown to retain substantial WT transcript, including SPINK1 c.194+2T>C, HBB c.315+2T>C, and BRCA2 c.8331+2T>C, illustrating how intermediate splicing effects complicate clinical interpretation across distinct genes and disease contexts. We then performed a locus-wide assessment of all 26 theoretically possible GT>GC substitutions in CFTR, integrating SpliceAI delta donor-loss scores with classifications from expert-curated databases. Minigene splicing analyses of four selected CFTR variants, together with full-length and minigene analyses of a BAP1 GT>GC variant with conflicting clinical interpretations, revealed heterogeneous and context-dependent splicing outcomes, underscoring both inter-assay variability and the inherent limitations of commonly used splicing assay systems. Collectively, our findings indicate that GT>GC variants capable of generating appreciable residual WT transcript exemplify a broader class of intermediate-effect alleles that expose the limitations of both computational prediction and experimental assessment. These observations highlight the need for classification frameworks that incorporate quantitative functional data and better capture the continuum of variant effects. - Source: PubMed
Publication date: 2026/04/01
Lin Jin-HuanWu HaoTang Xin-YingMasson EmmanuelleStenson Peter DPhillips Andrew DCooper David NFérec ClaudeLiao ZhuanZou Wen-BinChen Jian-Min - Pancreatic cancer remains one of the most intractable malignancies due to its strong therapeutic resistance and the difficulty of early detection. Previous studies have suggested that pancreatic inflammation can promote carcinogenesis. In contrast, the regulatory mechanisms controlling trypsin activity are closely associated with susceptibility to pancreatitis. Genetic variants that lead to sustained trypsin activity-thereby promoting protease activation-have been identified in hereditary pancreatitis. Serine protease inhibitor Kazal type 1 (SPINK1) functions as an endogenous inhibitor of trypsin activity. Deletion of Spink1 in mice causes severe pancreatic atrophy and early postnatal death. In addition to its role in pancreatitis, SPINK1 has been reported to exert cancer-promoting effects in several tumor types by supporting cell survival. - Source: PubMed
Publication date: 2026/03/19
Hayashi HidehiroHamada ShinMatsumoto RyotaroTakikawa TetsuyaXu YanJie RenNakasuji HitomiAbe ToshiakiKikuta KazuhiroMotohashi HozumiOhmuraya MasakiMasamune Atsushi