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Kruppel-like factor 15

KLF15, Kruppel-like factor 15
mouse homolog is a transcription factor that is an important regulator of the glucose transporter GLUT4 [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: CAN, V1a, ACID, Insulin, KLF2
Papers on KLF15
Uterine ALK3 is essential during the window of implantation.
Matzuk et al., Houston, United States. In Proc Natl Acad Sci U S A, Feb 2016
We determined that dual transcriptional regulation of Kruppel-like factor 15 (Klf15), by both the transforming growth factor β (TGF-β) transcription factor SMAD family member 4 (SMAD4) and progesterone receptor (PR), is necessary to inhibit uterine epithelial cell proliferation, a key step for embryo implantation.
c-Jun regulates adipocyte differentiation via the KLF15-mediated mode.
Bae et al., Taejŏn, South Korea. In Biochem Biophys Res Commun, Feb 2016
In addition, the expression level of KLF15, an upstream effector of the key adipogenic factors C/EBPα and PPARγ, was decreased upon the ectopic expression of c-Jun.
KLF15 Establishes the Landscape of Diurnal Expression in the Heart.
Jain et al., Cleveland, United States. In Cell Rep, Jan 2016
Here, we show that 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.
Glucocorticoids enhance muscle endurance and ameliorate Duchenne muscular dystrophy through a defined metabolic program.
Haldar et al., Copenhagen, Denmark. In Proc Natl Acad Sci U S A, Jan 2016
Here, we demonstrate that ergogenic effects of GCs are mediated by direct induction of the metabolic transcription factor KLF15, defining a downstream pathway distinct from that resulting in GC-related muscle atrophy.
Characterization of the promoter region of the bovine long-chain acyl-CoA synthetase 1 gene: Roles of E2F1, Sp1, KLF15, and E2F4.
Zhang et al., China. In Sci Rep, Dec 2015
Mutational analysis and electrophoretic mobility shift assays demonstrated that E2F1, Sp1, KLF15 and E2F4 binding to the promoter region drives ACSL1 transcription.
KLF15 Overexpression Protects β-Aminopropionitrile-Induced Aortic Rupture in Rodent Model via Inhibiting Connective Tissue Growth Factor.
Nie et al., China. In Thorac Cardiovasc Surg, Dec 2015
Lentivirus was used for in vitro and in vivo KLF15 overexpression in BAPN (β-aminopropionitrile)-induced rat AD models.
Branched-chain amino acids in metabolic signalling and insulin resistance.
Adams et al., United States. In Nat Rev Endocrinol, 2014
Research on the role of individual and model-dependent differences in BCAA metabolism is needed, as several genes (BCKDHA, PPM1K, IVD and KLF15) have been designated as candidate genes for obesity and/or T2DM in humans, and distinct phenotypes of tissue-specific branched chain ketoacid dehydrogenase complex activity have been detected in animal models of obesity and T2DM.
Novel excitation-contraction coupling related genes reveal aspects of muscle weakness beyond atrophy-new hopes for treatment of musculoskeletal diseases.
Brotto et al., Columbus, United States. In Front Physiol, 2013
In this review, we have focused on the unique function of new genes/proteins (i.e., MTMR14, MG29, sarcalumenin, KLF15) that during the last few years have helped provide novel insights about muscle function in health and disease, muscle fatigue, muscle metabolism, and muscle aging.
Kruppel-like factor 15 (KLF15) is a key regulator of podocyte differentiation.
He et al., New York City, United States. In J Biol Chem, 2012
a critical role of KLF15 in mediating podocyte differentiation and in protecting podocytes against injury.
KLF15 negatively regulates estrogen-induced epithelial cell proliferation by inhibition of DNA replication licensing.
Pollard et al., United States. In Proc Natl Acad Sci U S A, 2012
KLF15 is therefore a downstream physiological mediator of progesterone's cell cycle inhibitory action in the uterine epithelium.
Kruppel-like factor 15 regulates skeletal muscle lipid flux and exercise adaptation.
Jain et al., Cleveland, United States. In Proc Natl Acad Sci U S A, 2012
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
Klf15 orchestrates circadian nitrogen homeostasis.
Jain et al., Cleveland, United States. In Cell Metab, 2012
Nitrogen homeostasis exhibits circadian rhythmicity, and is orchestrated by Kruppel-like factor 15.
Circadian rhythms govern cardiac repolarization and arrhythmogenesis.
Jain et al., Cleveland, United States. In Nature, 2012
Specifically, we show that cardiac ion-channel expression and QT-interval duration (an index of myocardial repolarization) exhibit endogenous circadian rhythmicity under the control of a clock-dependent oscillator, krüppel-like factor 15 (Klf15).
Kruppel-like factor-15 inhibits the proliferation of mesangial cells.
Chen et al., Beijing, China. In Cell Physiol Biochem, 2011
KLF15 may be a useful target for therapeutic intervention in mesangial proliferative glomerulonephritis
Tapping the brake on cardiac growth-endogenous repressors of hypertrophic signaling.
Creemers et al., Amsterdam, Netherlands. In J Mol Cell Cardiol, 2011
In addition, we will focus on factors such as Kruppel-like factors (KLF4, KLF15 and KLF10) and histone deacetylases (HDACs), which constitute a relevant group of nuclear proteins that repress transcription of the hypertrophic gene program in cardiomyocytes.
Crosstalk between glucocorticoid receptor and nutritional sensor mTOR in skeletal muscle.
Tanaka et al., Tokyo, Japan. In Cell Metab, 2011
We identified direct target genes of the glucocorticoid receptor (GR) in skeletal muscle, i.e., REDD1 and KLF15.
Regulation of gluconeogenesis by Krüppel-like factor 15.
Jain et al., Boston, United States. In Cell Metab, 2007
KLF15 plays an important role in the regulation of gluconeogenesis.
Regulation of glucose transporter type 4 isoform gene expression in muscle and adipocytes.
Ahn et al., Seoul, South Korea. In Iubmb Life, 2007
These include MyoD, MEF2A, GEF, TNF-alpha, TR-1alpha, KLF15, SREBP-1c, C/EBP-alpha, O/E-1, free fatty acids, PAPRgamma, LXRalpha, NF-1, etc.
Mechanisms regulating GLUT4 glucose transporter expression and glucose transport in skeletal muscle.
Gumà et al., Barcelona, Spain. In Acta Physiol Scand, 2005
Recent information indicates that glut4 gene transcription is regulated by a number of factors in skeletal muscle that include MEF2, MyoD myogenic proteins, thyroid hormone receptors, Kruppel-like factor KLF15, NF1, Olf-1/Early B cell factor and GEF/HDBP1.
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