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
- Efficient lipid mobilization from yolk is critical for avian embryonic development, yet the cellular mechanisms governing lipoprotein transport in yolk sac membrane endodermal epithelial cells remain poorly characterized. Single-cell RNA sequencing was performed on 9,037 embryonic day 4 and 6,884 embryonic day 7 chicken yolk sac membrane cells to investigate lipoprotein biosynthesis pathways. Analysis identified 17 transcriptionally distinct clusters, including 3 endodermal epithelial cell subtypes. Cluster 2, characterized by high expression of epithelial markers (CDH1, EPCAM) and HDL biosynthesis genes (APOA1, ABCA1, LCAT), emerged as the primary site of HDL assembly. Apolipoprotein A1 ranked third in expression whereas apolipoprotein B ranked only 63rd, indicating a prominent HDL-biogenesis program in EECs. Gene ontology enrichment revealed upregulation of cholesterol metabolism and lipoprotein particle receptor binding pathways from embryonic day 4 to 7. Temporal expression analysis demonstrated progressive increases in HDL-related genes (APOA1, ABCA1, LCAT, SOAT1) throughout incubation, peaking at embryonic day 20, while VLDL-related genes (APOB, MTTP, SAR1B) showed sustained upregulation. Plasma analysis at embryonic day 19 confirmed HDL concentration (194.78 ± 30.13 mg/mL, mean ± SEM) significantly exceeded VLDL concentration (65.43 ± 13.82 mg/mL; P < 0.01), representing approximately 75% of measured lipoproteins. These findings reveal that HDL, rather than VLDL alone, plays a substantial role in lipid redistribution during late chicken embryogenesis, with HDL serving as the primary carrier of cholesteryl esters and phospholipids while VLDL remains the dominant triacylglycerol transporter, highlighting complementary lipoprotein functions and species-specific metabolic adaptations critical for embryonic development. - Source: PubMed
Publication date: 2026/04/17
Wu Jie-CiHu Zhao-QiLin Yuan-YuMersmann Harry JDing Shih-Torng - 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