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Validated All-in-One™ qPCR Primer for CD36(NM_001001547.3) Search again
Product ID:
HQP151166
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BDPLT10, CHDS7, FAT, GP3B, GP4, GPIV, PASIV, SCARB3
Gene Description:
CD36 molecule
Target Gene Accession:
NM_001001547.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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.
Gene References into function
- novel variants in individuals from malaria-endemic Ghana
- The metabolic role of CD36 was tested by glucose loading in type I or II CD36 deficiency pts. Changes in triglyceride and glucose metabolism were seen in CD36 deficiency due to impaired fast FA clearance by muscle and increased liver FA uptake.
- A redox-dependent conformational fraction of CD36, localized in the CD36 C-terminal cysteine-rich region, mediates cytoadherence of Plasmodium falciparum-infected erythrocytes to CD36-expressing cells and is inducible by low toxicity reducing agents.
- CD36 Pro90Ser mutation is not necessarily related to the insulin resistance syndrome, but is associated with high free fatty acid concentrations in Japanese
- CD36 deficiency induced by antiretroviral therapy.
- promoter structure and trans activation by pparalpha and ppargamma ligands
- Advanced glycation endproducts generated in situ are recognized by CD36, which might contribute to the pathogenesis of diabetic macrovascular complications.
- identification of terminal six amino acids of carboxy cytoplasmic tail as a functional domain implicated in binding and capture of oxidized low-density lipoprotein
- Genomic heterogeneity of type II CD36 deficiency
- Results offer structural insights into the molecular patterns recognized by the scavenger receptor CD36 and provide a platform for the development of potential therapeutic inhibitory agents.
- Heterozygotes, CD36+/-, have a significant reduction of long-chain fatty acids uptake in the heart independent of heart disease, suggesting genotype dependency and that CD36 might be a fundamental determinant of myocardial LCFA uptake.
- Data show that expression of CD36 on platelet membranes was increased in myeloproliferative, but was not significantly different from normal controls in non-insulin-dependent diabetes mellitus.
- mediates nonopsonic phagocytosis of erythrocytes infected with stage I and IIA gametocytes of Plasmodium falciparum in monocytes and macrophages
- Adhesion of dendritic cells derived from CD34+ progenitors to resting human dermal microvascular endothelial cells is down-regulated upon maturation and partially depends on CD11a-CD18, CD11b-CD18 and CD36.
- polySia of milk CD36 is significant for neonatal development in terms of protection and nutrition
- Macrophage recognition and phagocytosis of apoptotic fibroblasts is critically dependent on this protein.
- mediates endocytic uptake of advanced glycation end products
- Expression of the monocyte-macrophage LDL scavenger receptor CD36 is increased in people with diabetes mellitus, type 2.
- Expression in melanoma cells is regulated by NSAIDs.
- TSP-1-induced inhibition of megakaryocytopoiesis is probably mediated in part by the binding of TSP-1 to CD36 expressed on the megakaryocytic progenitors
- data suggest that platelet Cd36 has a key role in VLDL-induced collagen-mediated platelet aggregation, possibly contributing to atherothrombosis associated with increased VLDL levels
- Lipoprotein abnormalities in human genetic CD36 deficiency is associated with insulin resistance and abnormal fatty acid metabolism.
- Expression of CD36 mRNA was up-regulated by mildly- and moderately-oxLDL, but not highly-oxLDL.
- CD36 is localized in lipid rafts but not in caveolae, and binding of OxLDL to CD36 leads to endocytosis through a lipid raft pathway
- CD36 and SR-BI are receptors for hypochlorite-modified low density lipoprotein
- Higher levels of fatty acid translocase/CD36 in human female liver may aid sexually dimorphic development of diseases resulting from or characterized by disturbances in lipid metabolism, such as arteriosclerosis, hyperlipidemia, and insulin resistance.
- there is a CD36-dependent signaling cascade initiated by fibrillar amyloid species that may promote atherogenesis
- CD36 ribozyme specifically suppresses CD36 gene expression and growth in osteosarcoma csell lines.
- CD36 colocalizes with caveolin-3, suggesting that caveolae may regulate cellular fatty acid uptake by CD36. CD36 expression is higher in type 1 compared with type 2 fibers, whereas caveolin-3 expression is significantly higher in type 2 than in type 1
- CD36 was reactive with microvascular endothelium and adipocytes.Its expression on these high endothelial cells suggest that it participate in trafficking of leukocytes,especially lymphocytes to the omentum.
- CD36 is regulated by estrogen receptors in breast cancer cells
- CD36 has a role in beta-amyloid deposition but not with Alzheimer's disease
- Promoter polymorphism in CD36 is associated with atherogenesis is french population.
- Redistribution of FAT/CD36 to the sarcolemma may contribute to the etiology of insulin resistance in human muscle.
- A rare CD36 nonsense mutation found in a Caucasian pedigree with autosomal dominant type II diabetes.
- Single Nucleotide Polymorphisms in CD36 Antigens is associated with cardiovascular diseases
- In patients with type I CD36 deficiency, immunization with CD36 antigen by transfusion, can produce anti-CD36 antibody, and potentially lead to platelet transfusion refractoriness or post-tansfusion purpur
- host membrane proteins such as AE1 contribute to the adhesion of malaria-infected erythrocytes to CD36
- Single nucleotide polymorphism promoter mutation in the CD36 gene represents a putative genetic marker for insulin-resistance in the French population.
- CD36 activity appears important for uptake of fatty acids into beta-cells as well as for mediating their modulatory effects on insulin secretion.
- HIV-1 infection is associated with increased expression of CD36 on circulating monocytes; CD36 increased levels on monocytes could represent a proatherogenic condition in HIV-infected patients
- CD36 stimulated transport and consumption of palmitate and oleate, which they channeled away from complete oxidation and toward TAG synthesis.
- Up-regulation of CD36 may have a role in increasing oxidative stress in cultured microvascular endothelial cells and the heart in chronic diabetes.
- increase expression in an HIV infected pediatric population
- Myristic acid stimulates endothelial nitric-oxide synthase in a CD36- and an AMP kinase-dependent manner.
- binding of Plasmodium falciparum-infected erythrocytes to CD36 is increased in patients with South-Asian ovalocytosis genetic trait
- The effects observed at the level of CD36 scavenger receptor expression in vivo suggest an involvement of reduced foam cell formation in the protective effect of Vitamin E against atherosclerosis.
- specific amino acids of the C-terminal cytoplasmic tail of CD36 are crucial for the in vitro angiostatic activity of TSP-1
- CD36 may have a role in learning ability [review]
- CD36/FAT overexpression in familial combined hyperlipidemia occurs very early in adipocyte differentiation and may be of genetic origin
- Fatty acid transporter CD36 is involved in oral long-chain fatty acid detection; changes in pancreatobiliary secretions mediated by oral delivery of fatty acids are CD36-dependent
- A critical role for CD36 dephosphorylation through Src family kinase activation in regulating Plasmodium falciparum-infected erythrocytes adhesion to vascular endothelium was shown.
- Tissue-specific expression patterns of the alternative first exons of CD36 suggest that the alternative first exons of the gene are regulated individually and tissue specifically.
- cross-regulation of CD36 by PXR and PPARgamma suggests that this fatty acid transporter may function as a common target of orphan nuclear receptors in their regulation of lipid homeostasis
- interaction between cysteine interdomain region-1alpha and the host cell may be responsible for regulation of the CD4 T cell and cytokine responses to Plasmodium falciparum-infected erythrocytes reported previously
- cloned the cDNA for the induced mRNA in the mouse intestine and identified third promoter close to the first common exon of the gene. The human gene also has essentially the same gene organization
- In conclusion, the findings from this study indicate that exercise training alters the localization of FAT/CD36 and increases its association with CPT I, which may help augment fat oxidation.
- CD36 deficiency is accompanied by (1) hyperlipidemia and increased remnant lipoproteins, (2) impaired glucose metabolism based upon insulin resistance, and (3) mild hypertension
- Defects in CD36 have been linked to the hypertriglyceridemia and insulin resistance; this study using a rat model suggests that plasma glucose levels are more important in the regulation of expression than plasma insulin.
- TLR-2/6 and TLR2/1 heterodimer sorting at the cell surface determines heterotypic associations with CD36 and intracellular targeting
- CD36 expression is oppositely regulated compared to that of RUNX3 during monocyte-derived dendritic cell maturation, macrophage activation and myeloid cell line differentiation.
- CD36 binding activity is not critical for the oxPC-furan family of oxidized phospholipids
- sCD36 is related to risk factors of accelerated atherosclerosis in type 2 diabetes such as insulin resistance and glycemic control. sCD36 might represent a marker of the metabolic syndrome and a potential surrogate marker of atherosclerosis.
- Resistin promotes lipid accumulation in human macrophages through its upregulating CD36 cell surface expression.
- CD36 expression in childhood acute megakaryoblastic leukemia has a role in response to treatment
- In conclusion, CEOOH present in oxidized LDL increase CD36 gene expression in a pathway involving PPARalpha.
- Mitochondrial FAT/CD36 may be involved in regulating fatty acid oxidation in human skeletal muscle.
- CD36 selectively elicited lipid uptake from Cu(2+)-oxidized high density lipoprotein (HDL) but not from native HDL or low density lipoprotein (LDL).
- Glucose intolerance is associated with increased glycoxidation of circulating low density lipoproteins, which may contribute to the incireased expression of PPARgamma AND C36 in macrophages
- CD36-mediated fatty acid oxidation is an important determinant for aerobic exercise capacity in humans.
- There is a regulatory role of CD36-facilitated fatty acid uptake on adipocyte leptin expression, production, and signaling.
- CD36 mRNA decreased in idiopathic pulmonary fibrosis.
- Upregulation of CD36 in sporadic inclusion body myositis.
- platelet CD36 increase may be independent from the JAK2 V617F mutation in essential thrombocytopenia
- COX-2 induction is regulated by two sets of signaling mechanisms, one for the up-regulation of the scavenger receptor CD36 by HNE and one for the CD36-mediated COX induction by oxidized LDL
- Examine platelet GPIbalpha, GPIV and vWF polymorphisms and fatal pre-hospital myocardial infarction among middle-aged men.
- CD36, ICAM-1, and P-selectin are major contributors to the dynamic process of Plasmodium falciparum-infected red blood cell adhesion by different mechanisms in vivo
- These data therefore show that (i) Rab11a regulates cell surface abundance of both GLUT4 and FAT/CD36.
- Results suggested that the interaction between oxLDL and CD36 could be blocked using recombinant proteins and this may be useful in potential control of the trafficking of modified lipoproteins into monocytes leading to atherogenesis.
- A novel monocyte phenotype characterized by high TF/low CD36 presentation could be further developed for use as a marker for detection of individuals prone to developing prothrombotic conditions.
- Cd36 is a class B scavenger receptor that functions as a monomer to bind acetylated and oxidized low-density lipoproteins
- the (TG) repeat polymorphism in intron 3 of the CD36 gene is associated with a higher body mass index and cardiovascular risk for men in a Korean population
- Pioglitazone treatment reduced oluble CD36 while improving insulin-stimulated glucose metabolism in polycystic ovary syndrome.
- These results demonstrate the first evidence that the ligand activity of the advanced glycation end-products (AGE)-proteins to the scavenger receptors and its pharmacokinetic properties depend on their rate of modification by AGEs.
- CD36 mRNA expression is significantly increased in patients with coronary heart disease (CHD) and may serve as an indicator of CHD burden.
- C/EBPalpha regulates FAT/CD36 gene expression at the transcriptional level.
- oxPC(CD36) prevent binding to SR-BI of its physiological ligand, high density lipoprotein, because of the close proximity of the binding sites for these two ligands on SR-BI
- Scavenger receptor CD36 is implicated in retinal degeneration and choroidal involution, the cardinal features of the dry form of age-related macular degeneration.
- a segment within the C-terminal region of CIDRalpha determines CD36 binding specificity.
- CD36 variants may impact MetS pathophysiology and HDL metabolism, both predictors of the risk of heart disease and type 2 diabetes.
- fatty acids and insulin induce opposite alterations in CD36 ubiquitination, modulating CD36 level and fatty acid uptake
- in obese humans the FAT/CD36 protein content in skeletal muscle is dynamically regulated by insulin in vivo on the short term.
- These results suggest that LTA signaling preferentially occurs at the plasma membrane, is independent of internalization, and is facilitated by CD36 and CD14 as coreceptors for TLR2.
- results indicate that NAIT is caused by maternal CD36 deficiency having CD36 splicing abnormalities
- A CD36-dependent signaling cascade is responsible for oxLDL-dependent activation of platelets. It includes the src kinases Fyn and Lyn, the upstream MAP kinase kinase (MKK)4, and the MAP kinase JNK2.
- Novel evidence is provided that oxLDL induce a peroxisome proliferator-activated receptor gamma-independent CD36 overexpression, by up-regulating nuclear factor erythroid 2.
- SNPs in the CD36 gene modify the effects of fish oil on fasting plasma TAG, NEFA, glucose LDL and HDL cholesterol concentrations in healthy, middle-aged, Caucasian men.
- Filipin treatment rapidly increased the binding capacity of CD36 for the native lipoproteins HDL and LDL, but did not affect the binding capacity of CD36 for oxidized LDL
- Increased expression by OxLDL in PMA-differentiated THP-1 macrophages and in plaque vs. nonplaque lesion areas in human carotid endarterectomy specimens. The increase was correlated with higher ApoAI and lower HDL in plasma.
- VAR4 of Plasmodium falciparum is not involved in CD36 adhesion.
- CD36 functions as a phagocytic receptor for a variety of bacteria and mediates signaling induced by gram-negative bacteria and LPS via a JNK-mediated signaling pathway
- Association of CD36 exon 1a A allele with increased risk of severe malaria was observed.
- Data suggest that CD36 signaling in response to oxLDL alters cytoskeletal dynamics to enhance macrophage spreading, inhibiting migration, and possibly inducing trapping of macrophages in the arterial intima and promoting atherosclerosis.
- The effect of LDL particles showing extensive or low oxidation (HoxLDL and LoxLDL) on the expression of CD36 and FcgammaRII in a human monocytic cell line and the involvement of PPARgamma, was investigated.
- involved in MCP-1 and MIP-1b production by monocytes following OK-432 (lyophilized Streptococcus pyogenes) stimulation