GALNTL1 Blocking Peptide
- Known as:
- GALNTL1 Blocking Peptide
- Catalog number:
- 33r-5407
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- GALNTL1 Blocking Peptide
Related genes to: GALNTL1 Blocking Peptide
- Gene:
- GALNT16 NIH gene
- Name:
- polypeptide N-acetylgalactosaminyltransferase 16
- Previous symbol:
- GALNTL1
- Synonyms:
- KIAA1130, GalNAc-T16
- Chromosome:
- 14q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-30
- Date modifiied:
- 2015-09-11
Related products to: GALNTL1 Blocking Peptide
Related articles to: GALNTL1 Blocking Peptide
- Immune checkpoint inhibitors (ICIs) are widely used for treating hepatocellular carcinoma (HCC), yet their efficacy remains limited, with suboptimal response rates. The predictive power of the current biomarker, programmed death ligand-1 (PD-L1), is limited by detection variability and glycosylation, underscoring the need for complementary biomarkers to enhance predictive accuracy. In this study, mass spectrometry was employed to identify proteomic alterations in HCC tissues from responders and nonresponders to anti-programmed cell death-1 (PD-1) therapy. Survival analysis established the role of Yin Yang 1 (YY1) in determining ICI efficacy. Coculture models of hepatoma and CD8 T cells revealed the immunosuppressive function of YY1. Transcriptome sequencing identified polypeptide N-acetylgalactosaminyltransferase 16 (GALNT16) as a transcriptional target of YY1, and subsequent Western blot and coimmunoprecipitation assays demonstrated that GALNT16 augments PD-L1 expression. Furthermore, in vivo mouse models demonstrated that YY1 knockdown potentiated the efficacy of anti-PD-1 therapy, an effect that was partially reversed by GALNT16 overexpression. Specifically, YY1 upregulates GALNT16, which in turn promotes PD-L1 glycosylation and stability, leading to diminished CD8 T cell activity. Thus, GALNT16 knockdown rescued the compromised CD8 T cell cytotoxicity induced by YY1. Collectively, these results elucidate the YY1/GALNT16/PD-L1 axis as a pivotal mechanism underlying HCC resistance to ICI therapy. This highlights the therapeutic potential of targeting PD-L1 glycosylation pathways. - Source: PubMed
Publication date: 2025/11/26
Lin Shu-ShengXiao GangLiu Qin-QinXue Jia-HaoChen Zhi-JunZhang Hong-HuaZhu Xiang-PingHuang Keng-LongYang Cai-NiZhu KeLin Hao-MingZhang Rui - Bladder cancer is highly malignant, but specific biomarkers and molecular targets are lacking. The aim of this study was to screen bladder cancer progression-related differential genes based on those associated with tumor-node-metastasis (TNM) staging, and to validate them by and experiments. - Source: PubMed
Publication date: 2025/09/26
Ben LiangliangWang JianWu Peng - The aetiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), a chronic and severe debilitating disease with a complex phenotype, remains elusive. Associations with infectious diseases and autoimmune and neuropsychiatric disorders have been observed, without the identification of mechanisms. Previous studies suggest that genetic predisposition plays a role, but results are difficult to replicate, with Genome-Wide Association Studies of ME/CFS being challenging due to the relative rareness and heterogeneity of the disorder. We studied a well-defined Australian patient cohort diagnosed via the International Consensus Criteria, recruited by a specialist ME/CFS clinic. The whole-exome sequences of 77 patients were contrasted against genome variation in the 1000 Genome Project's genome-matched population. Significant associations with ME/CFS were harboured in genes that belong to the Neuroblastoma Breakpoint Family encoding Olduvai (DUF1220) domains, namely (rs3897177, -value = 3.15 × 10) (rs1553120233, -value = 9.262 × 10), and (rs200632836, -value = 1.04 × 10). Other significantly associated variants were detected in the , , , and genes, among others. Replication of these results was attempted via a GWAS on raw data from a US cohort, which confirmed shared significant associations with variation identified in the , , , , , , , and genes. These genes are involved in cortical neurogenesis, brain evolution, and neuroblastoma, and have been implicated by several studies in schizophrenia and autism. The sharing of these associations by the two cohorts supports their validity and grants the necessity of future studies to evaluate the implications for ME/CFS aetiology. - Source: PubMed
Publication date: 2025/06/17
Arcos-Burgos MauricioArcos-Holzinger MauricioMastronardi ClaudioIsaza-Ruget Mario AVélez Jorge ILewis Donald PPatel HardipLidbury Brett A - This study aimed to investigate the causal effect of plasma proteins on diabetic retinopathy (DR) risk and identify potential drug targets for this disease. - Source: PubMed
Liu HuanWang FeiyanHu ZiqingWei Jing - Schizophrenia is a complex neuropsychiatric disorder and heritability is as high as 80 % making it the most heritable mental disorder. Although GWAS has identified numerous variants, the pathophysiology is still elusive. Here, an attempt was made to identify genetic risk factors in familial cases of schizophrenia that are associated with a common causative pathway. To achieve this objective, exome sequencing was done in 4 familial cases and identified six unique coding variants in five genes. Among these genes, PIGQ gene has two pathogenic variants, one nonsense and in-frame deletion. One missense variant in GALNT16 and one in GALNT5 have variable damaging score, however, the other variants, in ADAMTS9 and in LTBP4 have the highest damaging score. Further analysis showed that the variant of LTBP4 was not present in the functional domain. The other missense variant in the ADAMTS9 gene was found to be significant and was present in the thrombospondin repeat motif, one of the important motifs. Detailed molecular dynamics simulation study on this variant showed a damaging effect on structural stability. Since, all these genes culminated into the glycosylation process, it was evident that an aberrant glycosylation process may be one of the risk factors. Although, extracellular matrix formation through glycosylation have been shown to be associated, the involvement of ADAMTS9 and PIGQ gene mediated glycosylation has not been reported. In this paper, a novel link between ADAMTS9 and PIGQ gene with schizophrenia have been reported. Therefore, this novel observation has contributed immensely to the existing knowledge on risk factor of Schizophrenia. - Source: PubMed
Publication date: 2023/04/25
Shekhar Bipin RajRupani KarishmaParkar Shubhangi RaghunathNayak Ajita SunilKumbhar Bajarang VasantKhare Satyajeet PMenon ShylaGawde HarshavardhanDas Dhanjit Kumar