Which key adipogenic transcription factors are down-regulated by Cucurbitacin E (CuE)?

Label:chem

Topic
Adipocyte differentiation is controlled by sequential activation of PPARγ and C/EBPα, master regulators of lipogenesis.
Answer
Western blotting and RT-PCR revealed that CuE markedly reduces mRNA and protein levels of PPARγ and C/EBPα, thereby inhibiting terminal adipocyte differentiation.
Return to Home Chemical List
Knowledge you may be interested in
How does CuE influence lipid accumulation in differentiating 3T3-L1 adipocytes? Does Cucurbitacin E (CuE) exhibit cytotoxicity toward 3T3-L1 adipocytes during adipogenesis? What is Cucurbitacin E (CuE) and where is it derived from? Is the antiviral activity of zinc ions maintained across physiologically relevant temperatures? Does zinc-mediated inactivation compromise the structural integrity of the IAV particle? How do zinc ions affect influenza A virus (IAV) hemagglutinin function and virus infectivity? What role does desloratadine or levocetirizine play when added to oral isotretinoin in the treatment of acne vulgaris? What evidence supports the efficacy of relugolix combination therapy in endometriosis? How do clinical outcomes compare between relugolix monotherapy and combination therapy? Does relugolix combination therapy preserve BMD over extended treatment periods? What molecular pathways are implicated in CuE-mediated inhibition of adipogenesis and lipogenesis? What is the overall conclusion regarding CuE’s potential as an anti-obesity agent? What is the role of synthetic angiotensin II (Giapreza®/AT2S) in the peri-operative management of kidney transplantation? Were there any safety concerns specific to angiotensin II (Giapreza®/AT2S) use? What is nicotine's proposed mechanism of neuroprotection in Parkinson’s disease (PD)? What were the findings of the meta-analysis regarding nicotine's effect on motor symptoms in PD patients? Did nicotine therapy improve activities of daily living (ADLs), quality of life (QoL), or cognition in PD patients? What limitations were identified in the clinical trials evaluating nicotine therapy for PD? What are the molecular targets of chlorogenic acid (CGA) and cinnamaldehyde (CA) in breast cancer cells? How strong are the binding interactions of CGA and CA with PI3K, Akt and PDK1 compared with FDA-approved drugs?