Ask about this productRelated genes to: SCARB1 antibody
- Gene:
- SCARB1 NIH gene
- Name:
- scavenger receptor class B member 1
- Previous symbol:
- CD36L1
- Synonyms:
- SRB1, CLA-1, CLA1, SR-BI
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-06
- Date modifiied:
- 2016-10-05
Related products to: SCARB1 antibody
Related articles to: SCARB1 antibody
- Retinal detachment (RD) remains an ophthalmologic emergency with high anatomical success rates after surgery but often suboptimal visual outcomes. This study aimed to identify transcriptomic signatures linked with clinical severity in human RD to uncover the molecular basis of variability in functional recovery. - Source: PubMed
Molinero-Sicilia LauraGalindo-Cabello NadiaRedruello-Guerrero PabloSobas-Abad Eva MaríaUsategui-Martín RicardoPastor-Idoate Salvador - This study aimed to assess the prevalence of genetic variants responsible for extreme levels of high-density lipoprotein cholesterol (HDL-C) and evaluate the adequacy of current thresholds for genetic testing of HDL-related dyslipidemia. - Source: PubMed
Publication date: 2026/04/20
Ølnes Åsa SchawlannTeigen MarianneStrøm Thea BismoArnesen Erik KristofferRimbert AntoineEggen Anne EliseBjune Katrine - Aberrant activation of the PI3K/AKT/mTOR signaling pathway is a common feature of cancer, but while mTOR kinase represents an attractive drug target, mTOR inhibitors have not seen broad success as single agents. To identify strategies to enhance the utility of third-generation bi-steric mTORC1 inhibitors, we performed genome-scale CRISPR interference chemogenomics screens, which revealed that mTORC1 inhibitor-mediated cytostasis leaves cells exquisitely dependent on the lipid peroxide scavenging enzyme GPX4. Mechanistically, using unbiased CRISPR activation chemogenomics screens, we demonstrate that mTORC1-dependent control of ferroptosis occurs, in part, through regulation of SCARB1 expression. Specifically, we find that the high-density lipoprotein (HDL) can suppress ferroptosis through interaction with its receptor SCARB1 and delivery of vitamin E to target cells. Our work highlights combining mTORC1 with GPX4 inhibition as one of the most promising combinatorial approaches for mTOR-targeted cancer therapies and defines an HDL-SCARB1 ferroptosis-suppression system that is regulated by mTORC1 activity. - Source: PubMed
O'Loughlin Thomas AStiles John SAcharya PritikaArab AbolfazlGoudy LaineDai RaymondBorah Ashir AWeiss William AMedoh Uche NGilbert Luke A - Diphenyltin (DPT) is an organotin and an endocrine disruptor, impairing the male reproductive system. However, the effect of DPT on Leydig cell function during puberty remains unknown. DPT exhibits selective testicular toxicity without altering gross reproductive organ weights. In rats administered 2.5-10 mg/kg DPT from postnatal day 35 to 57, serum testosterone levels were significantly reduced at 5 and 10 mg/kg, while luteinizing hormone and follicle-stimulating hormone levels remained unchanged. Histological and immunohistochemical analyses revealed decreased Leydig cell numbers and reduced expression of steroidogenic markers (STAR, LHCGR, SCARB1, CYP11A1, and INSL3). Testicular oxidative stress was evident, with downregulated SOD1, SOD2, and CAT and elevated malondialdehyde. Autophagy markers (LC3B, Beclin1) were upregulated alongside decreased phosphorylated mTOR, as well as increased 4-hydroxynonenal, 8-hydroxy-2'-deoxyguanosine, and LC3B staining in Leydig cells, suggesting oxidative stress-induced autophagy. In vitro, adult Leydig cells displayed ROS accumulation, mitochondrial membrane potential loss, and autophagosome formation. In adult Leydig cells, DPT enhanced mitochondrial fission by upregulating DRP1 and FIS1, downregulating MFN1, and activating PINK1-PARKIN-mediated mitophagy. The fission inhibitor mdivi-1 mitigated mitochondrial fragmentation, decreased mitophagy, and partially restored steroidogenesis. These findings indicate that DPT disrupts Leydig cell function through oxidative stress, mitochondrial fission, and mitophagy, ultimately leading to testosterone suppression and compromised sperm production. Therapeutic targeting of mitochondrial dynamics may protect steroidogenic cells from toxin-induced damage. - Source: PubMed
Publication date: 2026/04/12
Zhu QiqiYu JianqinChen NianciTian LiliHu ChunnanChen QuanxuZhu YangGe Ren-ShanLiu YiLi Xingwang - - Source: PubMed
Publication date: 2026/04/11
Altintas ZuhalCevik Muammer OzgurDerici Eker EbruAltintas Engin