mProX™ Human CD36 Stable Cell Line

Product Information

Target Family

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;HK-2

Target Classification

CD Cell Lines

Target Research Area

Cardiovascular Research

Related Diseases

Platelet Glycoprotein Iv Deficiency; Coronary Heart Disease 7

Gene ID

Human:948

UniProt ID

Human:P16671

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

CD36 is a protein that plays a role in various physiological processes. In the context of pulmonary arterial hypertension (PAH), CD36 is involved in metabolic signaling in right ventricle (RV) cardiomyocytes. Increased circulating leptin, which is associated with metabolic syndrome, can influence metabolic changes in RV cardiomyocytes via the CD36 receptor. Additionally, CD36 may alter lipid-dependent RV metabolism in combination with metformin in a mutation-specific manner. CD36 is also implicated in the maturation of lipid metabolism in the fetal and newborn sheep heart, as its gene expression progressively increases during the perinatal period. In the context of cancer, CD36 is involved in inhibiting cell proliferation in an inflammatory microenvironment by suppressing glycolysis and lipid metabolism. Furthermore, CD36 is linked to cholesterol deficiency in autism, as valproic acid exposure reduces CD36 protein levels in human microglial cells and neuroblastoma cells. Lastly, CD36 is a target for therapeutic efficacy in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), as mitochondria-targeted esculetin (Mito-Esc) administration regulates CD36 levels and improves lipid profile and glucose homeostasis. Overall, CD36 has diverse applications in various physiological and pathological conditions.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Skyler Smith (Verified Customer)

What is the role of CD36 in metabolic diseases and cancer? Jun 11 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

CD36 functions as a fatty acid translocase and is involved in lipid metabolism, playing a significant role in diseases like atherosclerosis, NAFLD, and cancer. Jun 11 2020

chat Alex Garcia (Verified Customer)

How does CD36 contribute to atherosclerosis? Jun 12 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

CD36 mediates the uptake of oxidized LDL, promoting foam cell formation and atherosclerotic plaque development, making it a target for atherosclerosis treatment. Jun 12 2022

Published Data

Fig.1 Immunofuorescence staining of CD36 in each group.

Lentivirus vectors (LV3-shRNA) were employed to construct CD36 expression knockdown, as confirmed through immunofluorescence staining. CD36 fluorescence manifestation was scarcely observed within the NG group. Following 72 h of HG stimulation, heightened CD36 fluorescence expression was induced. In the NG group, cytoplasmic distribution of fluorescence within HK-2 cells was noted; nevertheless, in the HG group, a tendency for fluorescence to be encompassed around the cell membrane was observed.

Ref: Hou, Yanjuan, et al. "CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys." Cell Death & Disease 12.6 (2021): 523.

Pubmed: 34021126

DOI: 10.1038/s41419-021-03813-6

Research Highlights

Talati, Megha. et al. "A potential adverse role for leptin and cardiac leptin receptor in the right ventricle in pulmonary arterial hypertension: effect of metformin is BMPR2 mutation-specific." Frontiers in medicine, 2023.
Pulmonary arterial hypertension (PAH) is a fatal cardiopulmonary disease. The relationship between the neuroendocrine hormone, leptin, which is released by adipose tissue, and cardiovascular diseases, including PAH, is complex.
Talati, Megha. et al. "A potential adverse role for leptin and cardiac leptin receptor in the right ventricle in pulmonary arterial hypertension: effect of metformin is BMPR2 mutation-specific." Frontiers in medicine, 2023.
Pubmed: 37869164 DOI: 10.3389/fmed.2023.1276422

R Drake, Rachel. et al. "Maturation of Lipid Metabolism in the Fetal and Newborn Sheep Heart." American journal of physiology. Regulatory, integrative and comparative physiology, 2023.
At birth, the fetus undergoes significant changes in its environment, accompanied by a shift in myocardial fuel preference from lactate and glucose in fetal life to fatty acid oxidation after birth. The researchers hypothesized that the fetal cardiac cells would mature in preparation for this extreme metabolic transformation during birth. The study quantified the expression of fatty acid transporters and enzymes before and after birth in sheep hearts. Results showed that several genes involved in fatty acid metabolism increased their expression during the perinatal period, while others remained stable during fetal life and increased after birth. Additionally, it was found that fetal cardiomyocytes had larger lipid droplets compared to newborn cardiomyocytes. These findings provide new insights into the perinatal development of cardiac fatty acid metabolism in a precocial species.
R Drake, Rachel. et al. "Maturation of Lipid Metabolism in the Fetal and Newborn Sheep Heart." American journal of physiology. Regulatory, integrative and comparative physiology, 2023.
Pubmed: 37867472 DOI: 10.1152/ajpregu.00122.2023