Recombinant Human SCARB1 /CD36L1 Protein
- Known as:
- Recombinant Human SCARB1 /CD36L1 Protein
- Catalog number:
- sc-797
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human SCARB1 /CD36L1 Protein
Related genes to: Recombinant Human SCARB1 /CD36L1 Protein
- 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: Recombinant Human SCARB1 /CD36L1 Protein
Related articles to: Recombinant Human SCARB1 /CD36L1 Protein
- 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 - (CT) infection is one of the most prevalent sexually transmitted infections (STIs) worldwide and has been consistently associated with adverse reproductive outcomes, including female infertility. However, the molecular mechanisms underlying this association remain incompletely understood. This study aimed to investigate whether genes previously associated with female infertility display altered expression patterns in response to CT infection by reanalyzing publicly available transcriptomic data derived from a human in vitro infection model. : An integrative in silico approach was employed. A curated list of 106 genes associated with female infertility was compiled from publicly available databases and integrated with transcriptomic data from the Gene Expression Omnibus (GEO) dataset GSE109428, which profiles primary human fallopian tube mesenchymal cells infected in vitro with CT serovar L2. Gene expression changes were evaluated at two time points (24 and 48 h post-infection) by comparing infected cells with uninfected control samples, followed by functional and phenotype enrichment analyses. : One female infertility-associated gene () was consistently dysregulated at both 24 and 48 h post-infection. In addition, fourteen genes (, , , , , , , , , , , , , and ) became significantly dysregulated exclusively at 48 h post-infection, indicating a time-dependent host transcriptional response to CT infection. Functional and phenotype enrichment analyses revealed associations with biological processes related to embryonic development and meiosis, as well as phenotypes linked to female infertility. These enriched terms were supported by a small subset of genes and were therefore interpreted cautiously. Overall, these findings suggest that CT infection modulates the expression of several infertility-associated genes and may influence biological pathways critical for female reproductive function. While exploratory, this study provides a molecular context that aligns with previously reported associations between CT infection and female infertility. - Source: PubMed
Publication date: 2026/03/01
Rodrigues RafaelaSousa CarlosVale Nuno