2016
DOI: 10.1016/j.bbrc.2015.12.035
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c-Jun regulates adipocyte differentiation via the KLF15-mediated mode

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Cited by 32 publications
(19 citation statements)
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“…Furthermore, different gene silencing techniques such as siRNA and shRNA, together with different transfection procedures (adenovirus, lentivirus transfection, and plasmid electroporation) have been applied to study the function of different genes associated with adipogenesis in 3T3-L1 cells. In particular, inflammatory pathways, adipokine synthesis, and secretion of study enzyme’s function have been investigated through gene silencing in adipocytes [ 43 , 44 , 45 , 46 , 47 ]. These cells have also been useful for deciphering the biological role of several miRNAs, such as miRNA-195a, which plays an essential role in various cellular processes including proliferation and differentiation [ 48 ].…”
Section: Animal Cell Modelsmentioning
confidence: 99%
“…Furthermore, different gene silencing techniques such as siRNA and shRNA, together with different transfection procedures (adenovirus, lentivirus transfection, and plasmid electroporation) have been applied to study the function of different genes associated with adipogenesis in 3T3-L1 cells. In particular, inflammatory pathways, adipokine synthesis, and secretion of study enzyme’s function have been investigated through gene silencing in adipocytes [ 43 , 44 , 45 , 46 , 47 ]. These cells have also been useful for deciphering the biological role of several miRNAs, such as miRNA-195a, which plays an essential role in various cellular processes including proliferation and differentiation [ 48 ].…”
Section: Animal Cell Modelsmentioning
confidence: 99%
“…KLF15 is directly induced by the glucocorticoid receptor, and glucocorticoid response element sites have been located within the first intron of the Klf15 gene (100) . c-Jun interrupts the glucocorticoid-mediated induction of KLF15 by occupying an intronic region near the glucocorticoid response element site of the Klf15 gene (102) . Thus, the browning of WAT is promoted by KLF11 and KLF15.…”
Section: Klf Biology In Organs Of Metabolic Interestmentioning
confidence: 99%
“…The glucocorticoid receptor activated KLF15 expression during adipogenesis of 3T3‐L1 (Sasse et al, ). The transcription factor c‐JUN was able to bind to Klf15 promoter near the glucocorticoid response element inhibiting the glucocorticoid stimulated adipogenesis (Lee et al, ), suggesting that a new branch of the transcriptional circuit might be targeting the expression of Pparg2 .…”
Section: Adipogenic Factorsmentioning
confidence: 99%