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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Kruppel-like factor 2

KLF2, LKLF, Kruppel-like factor 2
Kruppel-like factors (KLFs) are a family of broadly expressed zinc finger transcription factors. KLF2 regulates T-cell trafficking by promoting expression of the lipid-binding receptor S1P1 (S1PR1; MIM 601974) and the selectin CD62L (SELL; MIM 153240) (summary by Weinreich et al., 2009 [PubMed 19592277]).[supplied by OMIM, Feb 2011] (from NCBI)
Top mentioned proteins: V1a, CAN, KLF4, Nitric Oxide Synthase, HAD
Papers on KLF2
Cholecalciferol inhibits lipid accumulation by regulating early adipogenesis in cultured adipocytes and zebrafish.
Choi et al., Seoul, South Korea. In Biochem Biophys Res Commun, Feb 2016
CCF down-regulated the expressions of CCAAT-enhancer-binding protein-β (C/EBPβ), C/EBPδ, Krueppel-like factor (KLF) 4, and KLF5, while KLF2, a negative adipogenic regulator, was increased by CCF treatment.
The 11S Proteasome Subunit PSME3 Is a Positive Feedforward Regulator of NF-κB and Important for Host Defense against Bacterial Pathogens.
Wang et al., Shanghai, China. In Cell Rep, Feb 2016
PSME3, in turn, enhances the transcriptional activity of NF-κB by directly binding to and destabilizing KLF2, a negative regulator of NF-κB transcriptional activity.
Dopamine and T cells: dopamine receptors and potent effects on T cells, dopamine production in T cells, and abnormalities in the dopaminergic system in T cells in autoimmune, neurological and psychiatric diseases.
Levite, Jerusalem, Israel. In Acta Physiol (oxf), Jan 2016
ERK, Lck, Fyn, NF-κB, KLF2), (x) T cells produce dopamine (Tregs>>>Teffs), can release dopamine, mainly after activation (by antigen, mitogen, anti-CD3 antibodies, PKC activators or other), uptake extracellular dopamine, and most probably need dopamine, (xi) dopamine is important for antigen-specific interactions between T cells and dendritic cells, (xii) in few autoimmune diseases (e.g.
The KDM3A-KLF2-IRF4 axis maintains myeloma cell survival.
Anderson et al., Boston, United States. In Nat Commun, Dec 2015
Here we identify KDM3A-KLF2-IRF4 axis dependence in MM.
The transcription factor KLF2 restrains CD4⁺ T follicular helper cell differentiation.
Jameson et al., Minneapolis, United States. In Immunity, Mar 2015
Here we found that the KLF2 transcription factor serves to restrain Tfh cell generation.
Expression of Nitric Oxide-Transporting Aquaporin-1 Is Controlled by KLF2 and Marks Non-Activated Endothelium In Vivo.
Horrevoets et al., Amsterdam, Netherlands. In Plos One, 2014
The flow-responsive transcription factor Krüppel-like factor 2 (KLF2) maintains an anti-coagulant, anti-inflammatory endothelium with sufficient nitric oxide (NO)-bioavailability.
Capsaicin may have important potential for promoting vascular and metabolic health.
O'Keefe et al., Encinitas, United States. In Open Heart, 2014
TRPV1 activation induces calcium influx, and in certain tissues this is associated with increased activation or expression of key proteins such as endothelial nitric oxide synthase (eNOS), uncoupling protein 2 (UCP2), KLF2, PPARdelta, PPARgamma, and LXRα.
MicroRNA-92a Regulates Expression of Kruppel-like Factor2 in Rabbit Model of Intracranial Aneurysm.
Liu et al., Shanghai, China. In Cell Mol Biol (noisy-le-grand), 2014
To explore role of miRNA-92a in regulation of KLF2 expression in intracranial aneurysm model, real time PCR, IHC, ISH and luciferase activity were used to test relationship of miR-92a and KLF2.
Novel mechanisms of endothelial mechanotransduction.
Berk et al., Rochester, United States. In Arterioscler Thromb Vasc Biol, 2014
In contrast, steady laminar flow as atheroprotective flow promotes expression of many anti-inflammatory genes, such as Kruppel-like factor 2 and endothelial nitric oxide synthase and inhibits endothelial inflammation and athrogenesis.
Resetting transcription factor control circuitry toward ground-state pluripotency in human.
Smith et al., Cambridge, United Kingdom. In Cell, 2014
Here, we report that short-term expression of two components, NANOG and KLF2, is sufficient to ignite other elements of the network and reset the human pluripotent state.
Apelin-APJ signaling: a potential therapeutic target for pulmonary arterial hypertension.
Kim, Seoul, South Korea. In Mol Cells, 2014
There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Krűppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs).
Transcriptional downregulation of S1pr1 is required for the establishment of resident memory CD8+ T cells.
Jameson et al., Minneapolis, United States. In Nat Immunol, 2013
We found that CD8(+) T(RM) cells lacked expression of the transcription factor KLF2 and its target gene S1pr1 (which encodes S1P1, a receptor for sphingosine 1-phosphate).
The role of the transcription factor KLF2 in vascular development and disease.
Chico et al., Sheffield, United Kingdom. In Prog Mol Biol Transl Sci, 2013
The zinc-finger transcription factor KLF2 transduces the physical forces exerted by blood flow into molecular signals responsible for a wide range of biological responses.
Kruppel-like factor 1 (KLF1), KLF2, and Myc control a regulatory network essential for embryonic erythropoiesis.
Trudel et al., Richmond, United States. In Mol Cell Biol, 2012
The expression of the Myc gene is synergistically regulated by KLF1 and KLF2, and both factors bind the Myc promoters.
Myeloid-specific Krüppel-like factor 2 inactivation increases macrophage and neutrophil adhesion and promotes atherosclerosis.
Hui et al., Cincinnati, United States. In Circ Res, 2012
This study documents a role for myeloid KLF2 expression in modulating atherosclerosis.
Atheroprotective communication between endothelial cells and smooth muscle cells through miRNAs.
Dimmeler et al., Frankfurt am Main, Germany. In Nat Cell Biol, 2012
Data show that extracellular vesicles secreted by KLF2-transduced or shear-stress-stimulated umbilical vein endothelial cells (HUVECs) are enriched in miR-143/145 and control target gene expression in co-cultured smooth muscle cell (SMC).
Thioredoxin interacting protein promotes endothelial cell inflammation in response to disturbed flow by increasing leukocyte adhesion and repressing Kruppel-like factor 2.
Berk et al., Rochester, United States. In Circ Res, 2012
Thioredoxin interacting protein promotes endothelial cell inflammation in response to disturbed flow by increasing leukocyte adhesion and repressing Kruppel-like factor 2.
Kruppel-like factor 2 (KLF2) regulates monocyte differentiation and functions in mBSA and IL-1β-induced arthritis.
Das et al., Columbus, United States. In Curr Mol Med, 2012
The data provide new insights and evidences of KLF2-mediated transcriptional regulation of arthritis via modulation of monocyte differentiation and function.
The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.
Jain et al., Cleveland, United States. In Immunity, 2011
identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo
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