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)
- 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 - Disulfidptosis is a recently described cell-death-related process associated with intracellular disulfide stress and may be relevant to tumor progression and immune regulation. However, its prognostic significance and broader biological relevance in colorectal cancer (CRC) remain unclear. - Source: PubMed
Publication date: 2026/07/16
Zhou HuabinXiang SongruiWu YongjunLi ShipengZheng YuanchiLiu YulanZheng ChaoLi Min - Functionally defective genetic variants of the calcium channel transient receptor potential vanilloid type 6 (TRPV6) have been shown to markedly increase the risk for chronic pancreatitis in humans. Genetic inactivation of in mice worsened the severity of pancreatitis induced by secretagogue hyperstimulation. The aims of the present study were to reexamine the role of loss-of-function gene variants in an adult Hungarian cohort with nonalcoholic chronic pancreatitis and to characterize cerulein-induced pancreatitis in a novel -deleted mouse strain. We found that 2.1% of chronic pancreatitis patients carried defective variants, whereas no such variants were identified in control subjects. Homozygous deletion of in C57BL/6N mice () caused no spontaneous pancreatitis but slightly increased the severity of cerulein-induced acute pancreatitis and delayed recovery after an acute episode in a subset of mice. Cerulein-induced intrapancreatic trypsin and chymotrypsin activity was unchanged in mice relative to C57BL/6N controls. Crossing homozygous mice with heterozygous mice did not result in spontaneous pancreatitis. Our results confirmed the association of defective variants with human chronic pancreatitis in a nonalcoholic cohort. Furthermore, we found that TRPV6 played a relatively minor role in cerulein-induced murine pancreatitis, highlighting the need for better animal models for studying human variants. Prior studies indicated that defective variants of transient receptor potential vanilloid type 6 () encoding a constitutive calcium channel increased the risk of chronic pancreatitis in humans, and genetic inactivation of aggravated the severity of experimental pancreatitis in mice. We reexamined these findings by conducting a genetic case-control study and characterizing novel -deleted mice. We confirmed the association of defective variants with human chronic pancreatitis but found that deficiency had limited impact on secretagogue-induced pancreatitis in mice. - Source: PubMed
Publication date: 2026/07/07
Berke GergőSándor MátéRaheem SumiyyaMorales Granda Nataly CPesei Zsófia GabriellaHegede RékaDemcsák AlexandraNémeth Balázs CsabaWitt HeikoSzentesi AndreaHegyi PéterRohacs TiborHegyi EszterSahin-Tóth Miklós - Serine protease inhibitors of the Kazal type (Spinks) play important roles in protease regulation, blood coagulation, and immune responses. In this study, the spink1 gene from Pampus argenteus (Paspink1) was identified and characterized. The open reading frame (ORF) was 369 bp in length, encoding a polypeptide of 123 amino acids containing a typical Kazal domain. Recombinant protein PaSpink1 (rPaSpink1) was successfully expressed, and rPaSpink1 exhibited dose-dependent inhibitory activity against Trypsin and Proteinase K, as well as antibacterial activity against Staphylococcus aureus and Vibrio parahaemolyticus. Notably, although Paspink1 was predominantly expressed in the intestine, gill, and liver, its expression in the liver was significantly downregulated following V. parahaemolyticus infection, an alteration that correlated with increased hepatocyte apoptosis. Furthermore, this correlation was mechanistically validated in both in vivo and in vitro models. TUNEL-positive signals and upregulation of apoptosis-related genes were observed in vivo. In an in vitro Pampus argenteus liver (PAL) cell model, V. parahaemolyticus stimulation induced ROS accumulation and activated related signaling pathways of apoptosis. Importantly, overexpression of Paspink1 was associated with reduced ROS levels, as well as decreased apoptosis and inflammatory responses. These findings revealed that Paspink1 might play a protective role against bacterial infection by mitigating ROS-mediated apoptosis, providing new insights into the molecular mechanisms of disease resistance in aquatic organisms. - Source: PubMed
Publication date: 2026/06/30
Xue YadongZhou DianyangSun ZhennanYuan MingzheXie QingpingGuo ChunyangLiu XiumeiChen JianmingChang JingWang YajunZhou SumingWang Xubo - Clinical data show that genetic variants are significant risk factors for acute recurrent pancreatitis and chronic pancreatitis. To expand the understanding of the role of genetics in acute recurrent pancreatitis and chronic pancreatitis, high-throughput next-generation sequencing of 14 genes was completed in a multicenter pediatric cohort. - Source: PubMed
Publication date: 2026/06/16
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