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mouse homolog is a transcription factor that is an important regulator of the glucose transporter GLUT4. Additionally we are shipping and and many more products for this protein.
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In breast cancer cells, KLF6 (show KLF6 ELISA Kits) and KLF15 are suppressed via miR (show MLXIP ELISA Kits)-4262.
Findings suggest that, in obese status, the lower expression level of A2bAR (show ADORA2B ELISA Kits), KLF4 (show KLF4 ELISA Kits), and KLF15 of visceral adipose tissue may correlate with obese-dyslipidemia induced inflammation in Uygur population.
Case Reports: 2 girls with primary renal myoepithelial carcinomas with a novel EWSR1 (show EWSR1 ELISA Kits)-KLF15 fusion.
Our results indicate that nuclear KLF15 expression suppresses breast cancer cell proliferation at least partially through p21 (show CDKN1A ELISA Kits) up-regulation and subsequent cell cycle arrest
GR and KLF15 physically interact via low affinity GR binding sites within glucocorticoid response elements (GREs) for PRODH (show PRODH ELISA Kits) and AASS (show AASS ELISA Kits) that contribute to combinatorial regulation with KLF15.
KLF15 as a key regulator of myocardial lipid utilization and is the first to implicate the KLF transcription factor family in cardiac metabolism.
Host Kruppel-like factor 15, Slug, and SPDEF, stimulated the herpes simplex virus type 1 ICP0 promoter more than 150-fold.
A previously unrecognized KLF15-dependent pathway regulates vascular smooth muscle cell proinflammatory activation.
a critical role of KLF15 in mediating podocyte differentiation and in protecting podocytes against injury.
Elucidation of this heretofore unrecognized role for KLF15 now implicates this factor as a central component of the transcriptional circuitry that coordinates physiologic flux of all three basic cellular nutrients: glucose, amino acids, and lipids
Functional KLF15 significantly enhanced the promoter activity of fad24.
Kruppel-like factor 15 (KLF15) governs a biphasic transcriptomic oscillation in the heart with a maximum ATP production phase and a remodeling and repair phase corresponding to the active and resting phase of a rodent.
deletion of Klf15 interferes with nuclear control of mitochondrial fission, whereas fusion appears to be unaffected.
Our results demonstrate that c-Jun (show JUN ELISA Kits) can suppress adipocyte differentiation through the down-regulation of KLF15 at the transcriptional level.
KLF15 regulates bile acid synthesis via negative regulation of circadian Fgf15 expression.
Adipolin is transcriptionally regulated by KLF15 in adipocytes.
KLF15 upregulated slow myosin heavy chain expression through NFATc1 (show NFATC1 ELISA Kits).
This study establishes KLF15 as an important molecular link between ER stress and insulin (show INS ELISA Kits) action.
IL-17 (show IL17A ELISA Kits) suppresses expression of PPARgamma (show PPARG ELISA Kits), C/EBPalpha (show CEBPA ELISA Kits), KLF15, a pro-adipogenic transcription factor, and enhances expression of KLF2 (show KLF2 ELISA Kits) and KLF3 (show KLF3 ELISA Kits), which are anti-adipogenic.
The glucocorticoid receptor (show NR3C1 ELISA Kits) and KLF15 regulate gene expression dynamics, providing a novel mechanism for temporal control and signal integration by glucocorticoid receptor (show NR3C1 ELISA Kits).
mouse homolog is a transcription factor that is an important regulator of the glucose transporter GLUT4
Krueppel-like factor 15
, kidney-enriched Kruppel-like factor
, kidney-enriched krueppel-like factor
, cardiovascular Krueppel-like factor