Ask about this productRelated genes to: SAR1B antibody
- Gene:
- SAR1B NIH gene
- Name:
- secretion associated Ras related GTPase 1B
- Previous symbol:
- SARA2
- Synonyms:
- -
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-28
- Date modifiied:
- 2016-01-28
Related products to: SAR1B antibody
Related articles to: SAR1B antibody
- Conventional target screening repertoires provide limited coverage of proteome-level interactions, leaving critical gaps in the mechanistic toxicology of per- and polyfluoroalkyl substances (PFAS). In this study, thermal proteome profiling (TPP) was applied for unbiased, proteome-wide characterization of PFAS-protein interactions across five representative PFAS, identifying 173 proteins with significant ligand-induced stabilization. Specifically, legacy PFAS converged on small COPII coat GTPase SAR1A/SAR1B, consistent with potential mechanistic Target of Rapamycin (mTOR)-linked metabolic reprogramming, whereas the replacement ether PFAS hexafluoropropylene oxide dimer acid (HFPO-DA, commercially known as GenX) showed a distinct targetome highlighted by WD repeat-containing protein 89 (WDR89), suggesting non-nuclear-receptor mechanisms plausibly related to chromatin/complex assembly. Cellular thermal shift assay and molecular docking independently verified target engagement and provided a structural rationale for the observed stabilization patterns. Further ontology-based annotation linked the stabilized targets to 279 standardized disease entities, with a predominance of neoplastic outcomes. These findings demonstrate TPP as a new approach methodology for PFAS target discovery, reveal divergent early events for legacy versus replacement chemistries, and provide a proteome-scale framework to prioritize mechanism-based validation and to support evidence-weighted risk assessment of emerging fluorinated alternatives. - Source: PubMed
Publication date: 2026/03/26
Zheng XuehanLi YananQin HuaRuan ChengfeiYao LinlinLiu XianYe MingliangQu GuangboJiang Guibin - Chylomicron retention disease (CMRD) is a rare autosomal recessive disorder caused by pathogenic variants of , in which defective intestinal chylomicron secretion leads to fat malabsorption, hypocholesterolemia, and failure to thrive in infancy. Its diagnosis is typically challenging because of its rarity, nonspecific early symptoms, and overlap with other metabolic and malabsorptive disorders. The present case is notable for its neonatal onset with isolated failure to gain weight and the absence of persistent diarrhea or steatorrhea, complicating early clinical suspicion. Initial metabolic screening revealed overlapping abnormalities with urea cycle disorders and fatty acid oxidation defects, underscoring diagnostic complexity. A definitive diagnosis was achieved through the identification of compound heterozygous likely pathogenic variants, c.258G > A (p.Trp86Ter) and c.442C > T (p.Arg148Ter), thereby expanding the known phenotypic and genotypic spectrum of CMRD. The patient exhibited marked clinical and biochemical improvements following timely intervention with a low-fat, medium-chain triglyceride(MCT)-enriched diet and fat-soluble vitamin supplementation. However, subsequent follow-up revealed suboptimal adherence to the dietary regimen, leading to the emergence of typical steatorrhea, persistent growth failure, and neurodevelopmental delay, highlighting the critical and sustained role of strict nutritional management. This case highlights the importance of heightened clinical vigilance, timely genetic testing, and the necessity of ensuring long-term treatment adherence in infants presenting with unexplained growth failure and subtle hepatic abnormalities even when classic symptoms are absent. Taken together, this study provides valuable insights into the diagnostic challenges, therapeutic pitfalls, and management strategies of CMRD, emphasizing the need for multidisciplinary collaboration, enhanced awareness among clinicians, and further research to elucidate genotype-phenotype correlations and optimize patient care. - Source: PubMed
Publication date: 2026/02/12
Liu BingZhang Chunlei - Phospholipids serve as an efficient emulsifier and transport carrier for lipids. However, the regulatory mechanism by which phospholipids ameliorate lipid metabolic disorders induced by high-fat diet (HFD) remains unclear. The study aimed to investigate the effects and regulatory mechanisms of dietary phospholipids and HFD on intestinal lipid metabolism. We found that dietary phospholipids alleviated HFD-induced intestinal lipid deposition by inhibiting sterol regulatory element binding proteins 1 (SREBP1)-dependent lipogenesis and promoting peroxisome proliferator-activated receptor α (PPARα)-dependent lipolysis. Dietary phospholipids alleviated HFD-induced impairment in chylomicrons (CMs) synthesis and secretion by promoting microsomal triglyceride transfer protein (MTTP), apolipoprotein B and secretion-associated, Ras-related GTPase 1b (SAR1B) mRNA and protein expression. Moreover, dietary phospholipids alleviated the reduction in phosphatidylcholine synthesis induced by HFD via promoting cytidine triphosphate: phosphocholine cytidylyltransferase (CCTα) protein expression and mitigated HFD-induced ER stress by inhibiting glucose-regulated protein 78 (GRP78), protein kinase R like endoplasmic reticulum kinase (PERK) and activating transcription factor 4 (ATF4) mRNA and protein expression. Mechanistically, phosphatidylcholine promoted CCTα protein expression to alleviate the obstruction of CMs synthesis and secretion caused by fatty acid (palmitic acid and oleic acid). Moreover, phosphatidylcholine enhanced the transcription of mttp and sar1b genes by PPARα through reducing the interaction between ATF4 and PPARα, thereby promoting the CMs assembly and secretion to alleviate fatty acid-induced lipid deposition in primary intestinal cells of yellow catfish. Overall, this study reveals that phospholipids alleviate HFD-induced intestinal lipid accumulation through the ATF4-PPARα-MTTP/SAR1B pathway, and provides strong basis for phospholipids in the prevention of obesity-related metabolic diseases. - Source: PubMed
Publication date: 2026/01/06
Zheng HuaTan Xiao-YingWang BiaoZhong Chong-ChaoWei Xiao-LeiSong Chang-ChunLuo Zhi - Preterm (PT) infants are at increased risk for reduced postnatal lean mass accretion. We established that the feeding-induced stimulation of protein synthesis in skeletal muscle is blunted in piglets born PT compared with those born at term. - Source: PubMed
Publication date: 2025/12/27
Ramos Dos Santos Antonio CSuryawan AgusJang Ki BeomParada Rosemarie DMohammad Mahmoud AFiorotto Marta LDavis Teresa A - Perirenal fat deposition significantly impacts sheep carcass quality and economic efficiency. To elucidate the underlying genetic regulation, we performed a genome-wide association study (GWAS) on 556 Hu sheep and a comparative transcriptome analysis on 24 Hu sheep (12 with high- and 12 with low-perirenal fat deposition), all with accurate phenotypic records. Furthermore, hub genes and tissue-specific genes (TSGs) were discerned through weighted gene co-expression network analysis (WGCNA) and by leveraging RNA-Seq data from 12 tissues, respectively. qRT-PCR is used to validate the accuracy of RNA-Seq data. GWAS identified significant SNPs near genes including SETD4, TIMP2, SOCS3, and DNAH17. Comparative transcriptome analysis of HPF and LPF groups identified 2072 differentially expressed genes (DEGs), which were significantly associated with lipid storage (LPL), fatty acid homeostasis (APOE, GOT1), and biosynthesis (ACACA). A total of 2333 differential alternative splicing events were identified in 1169 genes, with skipped exons (SE, 30.65 %) being the most common. GO analysis of these SEs showed links to RNA splicing and lipid metabolism, with genes like BSCL2, DGAT1, PLIN5, and PNPLA2 involved in lipid droplet organization and triglyceride storage. WGCNA revealed key modules that were positively and negatively correlated with perirenal fat deposition, emphasizing hub genes (SAR1B, THRSP, ACSS2, KIF5B) associated with lipid droplet organization and metabolism. The integrated analysis of GWAS and RNA-seq identified TIMP2, SOCS3, and DNAH17 as potential key genes involved in regulating perirenal fat deposition in sheep. An association analysis of 372 Hu sheep populations identified significant links (P < 0.05) between perirenal fat deposition traits and mutations in the TIMP2 (g.9759169 G > A) and DNAH17 (g.9494469C > T) genes. Crucially, tissue-specific gene analysis across 12 tissues identified 448 perirenal fat TSGs, of which 75 were also differentially expressed genes (e.g., LPL, THRSP, LEP, ADRB3). In conclusion, our multi-omics study identified key genes influencing perirenal fat deposition in sheep. Notably, mutations in TIMP2 and DNAH17 could serve as candidate markers for enhancing carcass quality through marker-assisted selection. - Source: PubMed
Publication date: 2025/12/24
Fu XiaoyuZhao LimingTian HuibinZhang DeyinZhang YukunZhao YuanCheng JiangboLi XiaolongXu QuanzhongXu DanYang XiaobinMa ZongwuWu WeiweiLi FadiWang WeiminZhang Xiaoxue