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 >  Protein>CD36 >CD6-C52H6

Canine CD36 / SR-B3 Protein, His Tag

分子别名(Synonym)

CD36,SCARB3,BDPLT10,CHDS7,FAT,GP3B,GP4,GPIV,PASIV,Platelet Glycoprotein 4,glycoprotein IV,gpIV,glycoprotein IIIb,gpIIIb

表达区间及表达系统(Source)

Canine CD36, His Tag (CD6-C52H6) is expressed from human 293 cells (HEK293). It contains AA Gly 30 - Asn 439 (Accession # D5IGC7-1).

Predicted N-terminus: Gly 30

Request for sequence

蛋白结构(Molecular Characterization)

Online(Gly 30 - Asn 439) D5IGC7-1

This protein carries a polyhistidine tag at the C-terminus.

The protein has a calculated MW of 48.0 kDa. The protein migrates as 65-80 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>95% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

Canine CD36, His Tag (Cat. No. CD6-C52H6) SDS-PAGE gel

Canine CD36, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95%.

 
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背景(Background)

CD36 (Cluster of Differentiation 36) is also known as platelet membrane glycoprotein IV (GPIV), fatty acid translocase (FAT), thrombospondin receptor, collagen receptor, and scavenger receptor class B, member 3 (SRB3), is a member of the class B scavenger receptor family of cell surface proteins. The human CD36 gene encodes a single chain 472 amino acid residue protein containing both an N- and a C-terminal cytoplasmic tail and an extracellular loop.CD36 is found on platelets, erythrocytes, monocytes, differentiated adipocytes, mammary epithelial cells, spleen cells and some skin microdermal endothelial cells. CD36 is a multiligand pattern recognition receptor that interacts with a large number of structurally dissimilar ligands, including long chain fatty acid (LCFA), advanced glycation end products (AGE), thrombospondin-1, oxidized low-density lipoproteins (oxLDLs), high density lipoprotein (HDL), phosphatidylserine, apoptotic cells, beta-amyloid fibrils (fAβ), collagens I and IV, and Plasmodium falciparum infected erythrocytes. CD36 is required for the anti-angiogenic effects of thrombospondin1 In the corneal neovascularization assay. On binding a ligand the protein and ligand are internalized. This internalization is independent of macropinocytosis and occurs by an actin dependent mechanism requiring the activation Src-family kinases, JNK and Rho-family GTPases. CD36 ligands have also been shown to promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer.

 

 

前沿进展

Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease
Chen, Nisar, Mulla et al
EMBO Mol Med (2025)
Abstract: Global hepatic DNA methylation change has been linked to human patients with metabolic dysfunction-associated steatotic liver disease (MASLD). DNA demethylation is regulated by the TET family proteins, whose enzymatic activities require 2-oxoglutarate (2-OG) and iron that both are elevated in human MASLD patients. We aimed to investigate liver TET1 in MASLD progression. Depleting TET1 using two different strategies substantially alleviated MASLD progression. Knockout (KO) of TET1 slightly improved diet induced obesity and glucose homeostasis. Intriguingly, hepatic cholesterols, triglycerides, and CD36 were significantly decreased upon TET1 depletion. Consistently, liver specific TET1 KO led to improvement of MASLD progression. Mechanistically, TET1 promoted CD36 expression through transcriptional upregulation via DNA demethylation control. Overexpression of CD36 reversed the impacts of TET1 downregulation on fatty acid uptake in hepatocytes. More importantly, targeting TET1 with a small molecule inhibitor significantly suppressed MASLD progression. Conclusively, liver TET1 plays a deleterious role in MASLD, suggesting the potential of targeting TET1 in hepatocytes to suppress MASLD.© 2025. The Author(s).
Fat taste responsiveness, but not dietary fat intake, is affected in Adipor1 null mice
Lin, Gilbertson
bioRxiv (2025)
Abstract: Taste is a major driving force that influences food choices and dietary intake. Adiponectin has been shown to selectively enhance cellular responses to fatty acids by mediating the activation of AMPK and translocation of CD36 in taste cells via its receptor AdipoR1. Whether Adipor1 gene knockout affects fat taste responsiveness and dietary fat intake in animals remains unclear. In the present study, we evaluated cellular, neural, and behavioral responses to fat, as well as the dietary fat intake in global Adipor1 knockout mice and their WT controls. Sex-specific changes in cellular and behavioral responses to fatty acid were observed in Adipor1 knockout mice. Linoleic acid (LA)-induced calcium responsiveness appears to be reduced in taste cells from Adipor1 -deficient males and increased in taste cells from Adipor1 -deficient females. Brief-access taste testing revealed a loss of fat taste behavioral responsiveness in naïve Adipor1 -/- animals. Fat taste loss found in Adipor1 -/- males was restored after fat exposure and showed no significant differences in taste behavioral responses to fatty acids with WT controls in two-bottle preference and conditioned taste aversion tests. Adipor1 -/- females were found to have diminished preference for LA in two-bottle preference tests, lower intralipid/water lick ratio in a brief-access assay, and reduced avoidance for LA in conditioned taste aversion assay. Furthermore, the taste nerve responses to intralipid and the dietary fat intakes appeared to be the same between Adipor1 -/- and WT mice. In the high-fat diet feeding study, Adipor1 -/- females gained more weight, while no differences in body weight gain were found in males. Together, we show that adiponectin/AdipoR1 signaling plays crucial sex-specific roles in the modulation of fat taste and the maintenance of healthy body weight primarily by regulating energy expenditure rather than dietary fat intake in mice.
O-GlcNAc transferase-mediated O-GlcNAcylation of CD36 against myocardial ischemia-reperfusion injury
Zhao, Yan, Sun et al
Tissue Cell (2025) 95, 102878
Abstract: CD36 affects lipid metabolism and is involved in the development of myocardial infarction (MI). O-GlcNAcylation is a promising therapeutic target for myocardial ischemia-reperfusion (I/R) injury. This study aimed to investigate the effects of CD36 on myocardial I/R injury and its O-GlcNAcylation. H9C2 cardiomyocytes were induced by hypoxia/reoxygenation (H/R), and phenotypes were evaluated using cell counting kit-8, EdU assay, flow cytometry, and TUNEL assay. The O-GlcNAcylation was evaluated by immunoprecipitation, immunoblotting, and cycloheximide chase assay. The role of CD36 in vivo was analyzed by TTC staining and TUNEL assay. The results showed that CD36 protein levels were downregulated in I/R rats and H/R-induced H9C2 cells. OGT and O-GlcNAcylation levels were decreased by H/R. Overexpression of CD36 or OGT promoted cell proliferation and inhibited apoptosis of H/R-treated cells. Moreover, OGT facilitated the O-GlcNAcylation of CD36 at S195 site and enhanced CD36 protein stability. Knockdown of CD36 abrogated the effects of cellular behaviors caused by OGT, and CD36 mutation at S195 site reversed the promotion of proliferation and lipid uptake and the inhibition of apoptosis induced by wild-type CD36. Additionally, overexpression of CD36 attenuated infarction and apoptosis in the myocardium of rats. In conclusion, OGT-mediated O-GlcNAcylation of CD36 attenuates myocardial I/R injury through promoting the proliferation and inhibiting apoptosis of cardiomyocytes. The findings suggest that targeting CD36 O-GlcNAcylation may be a promising therapy for MI.Copyright © 2025. Published by Elsevier Ltd.
Showing 1-4 of 8989 papers.
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CD36靶点信息
英文全称:Platelet glycoprotein 4
中文全称:血小板糖蛋白4
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:0详情
最高研发阶段:临床前
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