PDIA6 Antibody
- Known as:
- PDIA6 Antibody
- Catalog number:
- XW-8125
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PDIA6 Antibody
Related genes to: PDIA6 Antibody
- Gene:
- PDIA6 NIH gene
- Name:
- protein disulfide isomerase family A member 6
- Previous symbol:
- TXNDC7
- Synonyms:
- P5, ERp5
- Chromosome:
- 2p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-11
- Date modifiied:
- 2015-11-16
Related products to: PDIA6 Antibody
Related articles to: PDIA6 Antibody
- Acute pancreatitis is a systemic inflammatory response that has the potential to affect numerous organs, resulting in persistent multiorgan failure and necrosis of the pancreas. According to previous studies, the development and occurrence of acute pancreatitis are linked to ferroptosis and immune responses. We assessed and validated the function of ferroptosis-related genes in acute pancreatitis and their association with inferred immune infiltration using bioinformatic analyses. Ferroptosis-related differentially expressed genes were identified using the Gene Expression Omnibus databases (GSE109227, GSE121038, and GSE183158) in conjunction with our transcriptome sequencing data. The involvement of ferroptosis-related differentially expressed genes was clarified through gene ontology, differential gene correlation, and gene set enrichment analysis. CIBERSORT analysis was used to evaluate and internally validate the immune microenvironment in acute pancreatitis. Comparative analysis of sequencing data from the pancreatic and liver tissues revealed 13 ferroptosis-related differentially expressed genes in acute pancreatitis. Gene ontology analysis primarily identified enrichment for iron ions, protein phosphatase, and actin filament binding. Gene set enrichment analysis predominantly highlighted the interleukin-18 and interleukin-23 pathways. Hub genes in the protein-protein interaction network included Egfr, Fads1, Hsp90b1, Krt18, Lcn2, Myh9, Pdia6, and Sqle. We identified 80 miRNAs, 67 transcription factors, and 24 potential drugs or molecular compounds associated with acute pancreatitis pathology. Quantitative reverse transcription polymerase chain reaction performed on caerulein-induced acute pancreatitis mouse models confirmed significant downregulation of Fads1, Hsp90b1, Pdia6, Sqle, and Cisd1 mRNA levels while showing significant upregulation of Osbpl9, Myh9, and Zfp36 mRNA levels. These findings suggested that these genes may represent candidate genes associated with AP and ferroptosis. Thirteen ferroptosis-related differentially expressed genes were discovered within the framework of acute pancreatitis, and their association with immune cell infiltration was studied. Future investigations should explore the possibility of Fads1, Hsp90b1, Pdia6, Sqle, Cisd1, Osbpl9, Myh9, and Zfp36 as novel therapeutic targets. - Source: PubMed
Publication date: 2026/04/29
Liu HuiYue MengliChen ShangsiLiu Pi - Metabolic dysfunction-associated steatohepatitis (MASH) is the most prevalent chronic liver disease worldwide; however, few effective therapeutic options are available for MASH. is a medicinal plant that has been widely utilized in traditional medicine to treat liver-related ailments. Nonetheless, the effects and underlying mechanisms of in the context of MASH remain poorly understood. - Source: PubMed
Publication date: 2026/04/15
Wang LinlinMiao YuWang HailongHasimu HamulatiJi TengfeiHuang HuaDu GuanhuaAisa Haji AkberXin Xuelei - Altered proinsulin levels in β-cells and bloodstream are hallmarks of diabetes and other diseases, but our knowledge about the proinsulin regulators remains limited. Here we perform a genome-wide CRISPR screen to identify 84 proinsulin regulators that alter intracellular proinsulin/insulin ratio in a mouse β-cell line. The proinsulin regulators are distinct from the insulin regulators from a previous orthogonal CRISPR screen. Functional annotation of the proinsulin regulators highlights Golgi as the primary organelle for proinsulin storage and regulation. Trafficking towards the Golgi increases the intra-cellular proinsulin/insulin ratio, while trafficking away from the Golgi, including exocytosis and Golgi-to-ER retrograde transport, decreases the intracellular proinsulin levels. We also map mouse quantitative trait loci (QTLs) associated with plasma proinsulin levels and use the CRISPR screen results to pinpoint the causal genes within the QTL loci. Interestingly, protein disulfide isomerase Pdia6 is the strongest hit from both CRISPR screen and the in vivo QTL mapping. Knocking down Pdia6 significantly reduce proinsulin accumulation in Golgi and secretory granules. Intriguingly, Pdia6-depletion in both human and mouse β-cells does not affect the folding status of proinsulin but causes significantly impaired proinsulin production through a UPR-independent mechanism. Taken together, our genetic profiles provide mechanistic insights into the regulation of proinsulin/insulin homeostasis. - Source: PubMed
Publication date: 2026/04/13
Lai SisiKeller Mark PZhang JinglinFang ZhouXie YingWeng ChenZhang SaixianZhang ShanshanGao PeidongKe LuxinWang YuntongMitok Kelly AClark LaurenSchueler Kathryn LLiu HanxiaoHatipoglu BetulHatzoglou MariaChen YuanyuanShalev AnathJin FulaiAttie Alan DLi Yan - Gastric cancer is one of the most prevalent cancers worldwide and is associated with a high mortality rate. Although immunotherapy has achieved some success for many tumor types, the limited response of gastric cancer to immunotherapy poses a challenge. Lactylation is a recently proposed post-translational modification derived from lactate that plays a key role in many physiological processes. In this study, we found that endoplasmic reticulum stress (ERS)-induced histone lactylation attenuated the immune response of dendritic cells (DC), decreased the ability of T cells to kill tumor cells, and enhanced tumor growth. Interestingly, ERS-induced H4K12 lactylation promoted the expression of PDIA6 in DC, leading to weakened immune activity of DC and decreased anti-tumor ability of T cells, thereby promoting gastric cancer immune evasion. Collectively, our work provides new insights into how ERS-induced lactylation modification attenuates the stability of DC to drive immune escape in gastric cancer and provides a promising biomarker for the efficacy of immunotherapy in gastric cancer. - Source: PubMed
Publication date: 2026/03/27
Tu ChengshuWu ZiqingZhong XuxianYang ShengnanChen XiLi SiminXu YouqinZuo Qiang - Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by hepatocyte ballooning, inflammation, and varying degrees of fibrosis. Protocatechuic acid (PCA), a naturally occurring phenolic compound found in many fruits and vegetables, exhibits various pharmacological properties. However, the precise mechanisms and molecular targets for MASH treatment remain unclear. In this study, we demonstrate that PCA ameliorates hepatic steatosis, fibrosis, and inflammation in MCD-fed mice and reduces lipid accumulation in hepatocytes via the IRE1-XBP1s signaling pathway. By using activity-based protein profiling (ABPP), we revealed that PCA binds protein disulfide isomerase A6 (PDIA6). Co-immunoprecipitation mass spectrometry (Co-IP-MS) analysis demonstrates that PCA enhances the interaction between PDIA6 and IRE1. This interaction suppresses the IRE1-XBP1s signaling pathway, reduces endoplasmic reticulum stress, and contributes to an anti-lipid deposition effect. PDIA6 knockdown inhibits lipid accumulation and eliminates the therapeutic impact of PCA. Collectively, these findings identify PDIA6 as a novel pharmacological target for PCA in the treatment of MCD-induced MASH, while advancing our understanding of disease pathogenesis. - Source: PubMed
Publication date: 2026/03/13
Hu HonglingLiao JiaxianYang ShiguangLi WenhuiFeng ShaZhang YuxueLin QiyueHuang JingnanHe WeiyiLiu DandanGao LeiZhang QianLuo PiaoWang Jigang