Ask about this productRelated genes to: HDLBP antibody
- Gene:
- HDLBP NIH gene
- Name:
- high density lipoprotein binding protein
- Previous symbol:
- VGL
- Synonyms:
- HBP
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-12-01
- Date modifiied:
- 2015-09-11
Related products to: HDLBP antibody
Related articles to: HDLBP antibody
- High-density lipoprotein-binding protein (HDLBP), also called Vigilin, is a multifunctional RNA-binding protein with established roles in RNA transport and regulation, chromosome segregation, lipid homeostasis, and translational regulation. Frequently detected to be perturbed in phosphoproteome analysis, phosphorylation is indicated as a major mechanism in the regulation of HDLBP functions; however, its phosphorylation landscape remains unexplored. We performed a meta-phosphoproteome analysis of HDLBP to map site-specific functional and regulatory roles of its two most frequently detected phosphosites, S31 and S944. Co-occurrence analysis across multiple datasets indicated that they can be phosphorylated together, suggesting potential co-ordinated regulation. Site-specific co-regulation analysis revealed distinct phospho-regulatory networks, with upstream kinases identified exclusively for S944. Functional enrichment of co-regulated protein phosphosites (CPPs) highlighted its role in RNA metabolism, chromosome organization, and nucleoplasmic transport, while functional annotation of site-specific phosphorylation of CPPs indicates its involvement in cell cycle regulation, apoptosis, and carcinogenesis. Additionally, the potential role of CPPs in the lipid homeostasis network was explored. Furthermore, the differential expression of HDLBP phosphosites across multiple cancers was observed using UALCAN, suggesting a potential role for phospho-regulation of HDLBP in tumor-associated pathways. Together, these findings provide the first integrated view of HDLBP phosphorylation and could serve as a valuable framework for future targeted studies to elucidate the mechanistic roles of site-specific HDLBP phosphorylation in cellular and pathophysiological processes. - Source: PubMed
Publication date: 2026/02/25
Sekhar Pathiyil SajiniFahma AmalSubair SuhailDcunha LeonaMahin AlthafGopalakrishnan Athira PerunallyRaju RajeshSoman Sowmya - In pancreatic ductal adenocarcinoma, hypoxia is a crucial component of the tumour microenvironment and is associated with worse clinical outcomes. Adaptation to extreme hypoxic settings is based on abnormal lipid metabolism, but insights into how hypoxia-regulated lipid changes link with aggressive migratory potential in pancreatic cancer are lacking. This study investigates the molecular processes, pathways, and critical proteins involved in hypoxia-induced lipidic and polyunsaturated fatty acid alterations in pancreatic cancer. Our findings elucidate increased multilayer unsaturation in FA chains of major lipid classes associated with greater migration and invasion, as well as higher abundances of particular desaturases. The expression of these proteins was verified in clinical tumour samples by unsaturated fatty acid biosynthesis-related gene enrichment score. High unsaturated fatty acid clusters were shown to be associated with a low survival rate. Pathway correlation and protein-protein interaction analysis indicated that the PPAR-hypoxia axis and SCD/FADS2/APOC3-HDLBP protein network are implicated in mediating the observed alterations in lipid pools and poly-unsaturation levels in pancreatic cancer under hypoxia. These results provide novel therapeutic targets in pancreatic cancer while improving our understanding of hypoxia-induced migratory potential in pancreatic cancer. - Source: PubMed
Publication date: 2025/12/01
Agarwala Prema KumariSingh AvinashSrivastava SanjeevaKapoor Shobhna - As one of the most prevalent malignancies worldwide, colorectal cancer (CRC) exhibits a strong metabolic dependency on glycolysis, which fuels tumor expansion and shapes an immunosuppressive microenvironment. Despite its clinical significance, the regulatory landscape and cellular diversity of glycolytic metabolism in CRC require systematic exploration. Multi-omics datasets (bulk/scRNA-seq and spatial transcriptomics) were analyzed to quantify glycolytic signatures. Core regulatory genes were selected via integrated pathway mapping and a machine learning framework incorporating five-feature selection algorithms. Cellular subpopulations were delineated by metabolic profiles, with niche interactions modeled through ligand-receptor network analysis. Findings were validated across multicenter cohorts. Our analyses identified a tumor subpopulation characterized by a High Glycolytic State (HGS), displaying elevated glycolytic signature alongside stem-like properties. Spatial profiling demonstrated relative enrichment of HGS cells in central tumor regions, potentially reflecting adaptation to nutrient-limited conditions. Among the molecular features associated with HGS maintenance, five candidate regulators (PFKP, ERO1A, FKBP4, HDLBP, HSPA5) showed correlation with unfavorable clinical outcomes. Our study characterizes the metabolic heterogeneity of CRC and suggests a potential role for HGS cells in shaping the tumor microenvironment. The molecular features identified here may offer insights into metabolic dependencies that could be explored for future therapeutic targeting. - Source: PubMed
Publication date: 2025/08/30
Du YuanyuanMiao ZefengLi PengFeng DanLiu MulinJi AifangLi Shijun - Somatic mutations that increase clone fitness or resist disease are positively selected, but the impact of these mutations on organismal health remains unclear. We previously showed that Tbx3 deletion increases hepatocyte fitness within fatty livers. Here, we detected TBX3 somatic mutations in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). In mice, Tbx3 deletion protected against, whereas Tbx3 overexpression exacerbated, MASLD. Tbx3 deletion reduced lipid overload by accelerating VLDL secretion. Choline-deficient diets, which block VLDL secretion, abrogated this protective effect. TBX3 transcriptionally suppressed the conventional secretory pathway and cholesterol biosynthesis. Hdlbp is a direct target of TBX3 that is responsible for the altered VLDL secretion. In contrast to wild-type TBX3, the TBX3 I155S and A280S mutations found in patients failed to suppress VLDL secretion. In conclusion, TBX3 mutant clones expand during MASLD through increased lipid disposal, demonstrating that clonal fitness can benefit the liver at the cost of hyperlipidemia. - Source: PubMed
Publication date: 2025/07/10
Mannino GregoryQuinn GabriellaZhu MinWang ZixiWang XunLi BoyuanHsieh Meng-HsiungMathews ThomasZacharias LaurenGu WenGopal PurvaBrzozowska NataliaCampbell PeterHoare MattLiszczak GlenZhu Hao - Gap junction protein β2 (GJB2) has been associated with glycolysis and immunosuppression in human tumors. This research aims to explore the roles of GJB2 in these aspects in the context of lung adenocarcinoma (LUAD). GJB2 expression in LUAD was analyzed using bioinformatics tools and verified in human LUAD cells. RNA binding proteins that target GJB2 were predicted using bioinformatics and verified using RNA immunoprecipitation assays. Gain- or loss-of-function assays of GJB2 and high-density lipoprotein binding protein (HDLBP) were performed in LUAD cells to investigate their roles in glycolysis. These LUAD cells underwent coculture with activated CD8 T cells to examine the effect of gene interference on the exhaustion and activity of T cells. A mouse model of allograft tumor was established for validation. GJB2 exhibited aberrantly heightened expression in LUAD cells. Further overexpression of GJB2 in cancer cells increased glucose uptake, lactate production, and extracellular acidification rate; augmented aggressive phenotype of cancer cells; and increased exhaustion of the cocultured CD8 T cells. HDLBP, an RNA binding protein that binds to GJB2 RNA, was found to be highly expressed in LUAD as well, which enhanced GJB2 expression by stabilizing the GJB2 mRNA. Overexpression of HDLBP similarly rendered glycolysis and T cell inactivity, with these effects negated by GJB2 knockdown. In parallel, GJB2 silencing in mouse 3LL cells suppressed tumorigenesis, glycolysis, and T cell exhaustion in mice promoted by HDLBP. This research suggests that HDLBP-mediated GJB2 RNA stabilization augments glycolysis and CD8 T cell exhaustion in LUAD progression. - Source: PubMed
Xu LiZhou BinJin KaiqiGe TaoDeng MingDing HongdouXu Xinnan