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Human CD36 Protein expressed in Human Cells - ABIN2003345
Xu, Efremov, Li, Lai, Dao, Lim, Cao: Probing the cytoadherence of malaria infected red blood cells under flow. dans PLoS ONE 2013
data suggest that the IVS4-10A allele of CD36 (rs3211892) is associated with a lower risk of hypercholesterolemia; data suggest a possible protective effect of a higher sCD36 concentration in relation to metabolic syndrome components
normal and defective embryos lacking SR-B1 have divergent expression profiles
CD36 plays an important role in the preabsorptive hormone and Bile acids responses that coordinate brain and gut regulation of energy metabolism.
We identified CD36 as one of the most significantly upregulated lipid-related genes in senescent cells. We showed that overexpression of CD36 in proliferating cells resulted in a senescence-like phenotype. We hypothesize that CD36 overexpression leads to changes in membrane remodeling and plausibly mediate SASP release.
Our findings indicated that hepatic stellate cells-derived COMP collaborated with CD36 and subsequently played an essential role in MEK/ERK and PI3K/AKT-mediated hepatocellular carcinoma (HCC) progression. COMP might act as a promising target for the diagnosis and treatment of aggressive HCC.
Study shows the CD36 expression level downregulated in the lung cancer. Further, results found that the high methylation of CD36 corresponding to its low expression in lung cancer played an important role in the procession of lung cancer.
The rs7755 and rs3211956 loci polymorphisms of CD36 gene and genotype E2/E3, E3/E4, E4/E4 of ApoE gene, and E2 and E4 alleles were statistically related with Alzheimer disease.
This study suggests that T2D patients with different genotypes at CD36, NOS3 and PPARG respond differentially to intervention of omega-3 supplements in blood lipid profiles.
Gene expressions of YKL-40 and CD36 were significantly higher in patients with T2DM (>5 yr) with hypertension compared to healthy controls (P=0.006). In addition, a significant increase in serum levels of sCD36, PPAR-gamma and YKL-40 was observed in patients with T2DM (>5 yr) with hypertension compared to healthy controls
genetic association studies in population of preschool-aged children in Guelph, Ontario: Data suggest that SNPs in CD36 (rs1761667), TAS1R2 (rs35874116), and TAS2R38 (rs713598) are associated with snacking behavior in the population studied. [PILOT PROJECTS]
CD36 is important for muscle glucose metabolism and optimal insulin responsiveness.
Significant up-regulation of PBMCs CAP1, CD36 mRNA and plasma resistin found in significant coronary artery disease, as well as in nonsignificant coronary artery disease compared to control group, indicates that resistin could be able to exert its effects stronger on cells with up-regulated CAP1 mRNA thus contributing atherosclerosis development.
CD36, also known as FA translocase (FAT), that functions as a transmembrane protein and mediates the uptake of FAs, is observed to be highly expressed in breast cancer tissues. Furthermore, the anti-proliferation effect caused by the SCD1 inhibitor can not be reversed by exogenous oleic acid supplementation in CD36 knockdown breast cancer cells
Results showed that CD36 genotypes were not associated with the progression to T2DM independently. however, the study suggested a positive interaction between the CD36 variants and obesity on T2DM susceptibility, which might be through a cardiometabolic disorder.
Taken together, these findings indicate that rs1194182 polymorphism in the CD36 gene was associated with intracerebral hemorrhage, and genotype GG could be an independent predictor.
Three polymorphisms were found to be associated with increases in IOP: rs1049673 (p = 0.006), rs3211931 (p = 0.01), and rs1761667 (p = 0.043) at the time of the third injection only.
CD36 marks adipocyte progenitor cells with pronounced adipogenic potential, most probably by facilitating lipid uptake.
sCD36 levels increased with the level of intrahepatic lipid, insulin resistance and dyslipidemia; association with markers of obesity and the association with hepatic CD36 mRNA expression suggest that excess sCD36 in NAFLD patients is derived from the hepatocytes, which may support that CD36 is involved in NAFLD development; an unhealthy CD36 expression in adipose and hepatic tissue may shift the fatty-acid load to liver
In conclusion, oxLDL induced MALAT1 transcription and MALAT1 recruits beta-catenin to binding sites on the CD36 promoter to induce CD36 expression, which enhances lipid uptake in macrophages.
Based on these findings, we conclude that an acetylation-deacetylation signaling step might regulate CD36 functional activity and subsequent lipid accumulation and caspase 3 activation in pancreatic beta cells exposed to GLT conditions.
Amyloid-beta inhibits No-cGMP signaling in a CD36- and CD47-dependent manner
Inhibition of hepatic scavenger receptor-class B type I by RNA interference alters lipoprotein metabolism and decreases atherosclerosis in rabbits.
Niacin Reduces serum level and adipose mRNA expression of leptin and up-regulates PPARgamma and CD36 mRNA expression in hypercholesterolemic rabbits.
Fndings suggest that CD36 antigen facilitates transfer of medullary thymic epithelial cells (mTECs)-derived cell-surface antigen on CD8alpha(+) dendritic cells (DCs) to promote tolerance to host antigens during allogeneic BM transplantation (allo-BMT).
Disturbed flow facilitates endothelial CD36-dependent uptake of oxidized lipids resulting in local increase of endothelial stiffness in proatherogenic areas of the aorta.
SIRT1 upregulation protects against liver injury induced by a HFD through inhibiting CD36 and the NF-kappaB pathway in mouse Kupffer cells.
Cd36 deficiency led to reduced expression of phagocytosis receptor Mertk and nuclear receptor Nr4a1 in cardiac macrophages, the latter previously shown to be required for phagocyte survival.
CD36 plays an important proinflammatory role in ConA-induced liver injury by promoting hepatic inflammation and mediating the proapoptotic effect of chemokine CXCL10, and therefore, may be a potential therapeutic target for immune-mediated hepatitis
both paracrine and endocrine effects of adiponectin may contribute to reduced reactive oxygen species generation and apoptosis after MI/R, in a CD36-dependent manner
Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE(-/-) /LDLR(-/-) mouse via a PPARgamma/CD36 pathway.
This study demonstrated the CD36 deletion in mice (CD36(-/-) mice) resulted in an attenuated progression of chronic epilepsy compared with wild-type (WT) mice.
TMP upregulated the protein stability of ABCA1 without affecting ABCG1. Accordingly, TMP regulated the expression of SR-A, CD36, ABCA1 and ABCG1 in aortas of ApoE-/- mice, which resembled the findings observed in macrophages.
atherogenic condition could activate eosinophils and modulate the phenotype of macrophages (from M2 to M1 phenotype), in part, through the CD36 receptor signaling
CD36 plays a role in the perception of specific odour-active volatile compounds in the nasal cavity.
CD36 plays an important role in modifying gallstone susceptibility in mice
CD36 is essential for endurance improvement, changes in whole-body metabolism, and efficient peroxisome-proliferator activated receptors (PPAR)-related transcriptional responses in the muscle with exercise training.
development of obesity-related chronic kidney disease via CD36 in mice
The low magnitude of opsonin-independent phagocytosis of Escherichia coli and unimpaired phagocytosis of Staphylococcus aureus in SR-A- or CD36-deficient macrophages indicate that the defect in this process might not be responsible for the reported impaired bacteria clearance in mice deficient in these receptors.
Results show that CD36 deficiency promoted the development of nonalcoholic steatohepatitis by facilitating the transcription of MCP-1 in hepatocytes due to the reduction of ROS and nuclear HDAC2. These results provide evidence that decreased ROS production by CD36 deletion was also harmful for livers. The fine balance of CD36 plays an important role in maintaining balances of hepatic ROS and nuclear HDAC2.
Coexpression of the Olfr287 in olfactory sensory neurons with CD36 suggests that only a specific set of olfactory receptors may be coexpressed with CD36 in these neurons.
Neither the lack of CD36 nor the deletion of the smac gene from Plasmodium chabaudi significantly impacted on acute-stage pathology or parasite sequestration. By contrast, in the absence of ICAM-1, infected animals experience less anaemia and weight loss, reduced parasite accumulation in both spleen and liver and higher peripheral blood parasitaemia during acute stage malaria.
These results suggest that increased expression of hepatic CD36 and SREBP-1 is relevant in the obesity-driven lipid accumulation in the liver of dairy cows during late gestation.
Gammadelta T cells express CD36 and it contributes to responses by these cells to microbial lipoteichoic acid.
The findings of this study indicated that Cd36 is a candidate lipid sensor involved in the sensory detection of fatty acid in zebrafish.
Zebrafish Cd36 is a microbial-binding molecule.
The putative role for Cd36 in immune responses of fish in the context of other members of the scavenger receptor class B family, is discussed.
CD36 plays a vital role in the LPS-induced activation of downstream signaling cascades and mediates E. coli phagocytosis via TLR4 in pGMECs, which offers a novel treatment strategy for mastitis
The protein encoded by this gene is the fourth major glycoprotein of the platelet surface and serves as a receptor for thrombospondin in platelets and various cell lines. Since thrombospondins are widely distributed proteins involved in a variety of adhesive processes, this protein may have important functions as a cell adhesion molecule. It binds to collagen, thrombospondin, anionic phospholipids and oxidized LDL. It directly mediates cytoadherence of Plasmodium falciparum parasitized erythrocytes and it binds long chain fatty acids and may function in the transport and/or as a regulator of fatty acid transport. Mutations in this gene cause platelet glycoprotein deficiency. Multiple alternatively spliced transcript variants encoding the same protein have been found for this gene.
CD36 antigen (collagen type I receptor, thrombospondin receptor)
, PAS IV
, PAS-4 protein
, cluster determinant 36
, fatty acid translocase
, glycoprotein IIIb
, leukocyte differentiation antigen CD36
, platelet glycoprotein 4
, platelet glycoprotein IV
, scavenger receptor class B, member 3
, adipocyte membrane protein
, collagen type I receptor thrombospondin receptor
, fatty acid transport protein
, fatty acid translocase/CD36
, CD36 antigen
, collagen type I receptor, thrombospondin receptor