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Kruppel-like factors (KLFs) are a family of broadly expressed zinc finger transcription factors. Additionally we are shipping KLF2 Antibodies (98) and KLF2 Kits (7) and many more products for this protein.
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KLF2 expression was decreased in gastric cancer and negatively correlated with lymphatic metastasis. KLF2 overexpression inhibited cell proliferation and invasive potential and downregulated the protein expression of PCNA (show PCNA Proteins), Bcl-2 (show BCL2 Proteins) and MMP-9 (show MMP9 Proteins) in GC cells. KLF2 overexpression reduced xenograft tumor growth.
our data highlight an important role for KLF2/c-myc (show MYC Proteins) pathway in HCC (show FAM126A Proteins) development and progression.
Authors show that KLF2 induces the expression of CRABP2 (show CRABP2 Proteins) and RARgamma and inhibits the expression FABP5 (show FABP5 Proteins) and PPARbeta (show PPARD Proteins)/delta thereby shifting RA signaling from the pro-carcinogenic FABP5 (show FABP5 Proteins)/PPARbeta (show PPARD Proteins)/delta to the growth-suppressing CRABP2 (show CRABP2 Proteins)/RAR (show RARA Proteins) path.
MicroRNA-30 mediates anti-inflammatory effects of shear stress and KLF2 via repression of Ang2.
In hyperuricemia, miR (show MLXIP Proteins)-92a downregulation increased KLF2 expression, subsequently inhibiting VEGFA (show VEGFA Proteins), which resulted in decreased angiogenesis.
These data provide support for a continuous role of KLF2 in stabilizing the vessel wall via co-temporal expression of eNOS and AQP1 both preceding and during the pathogenesis of atherosclerosis.
These results indicate that the KDM3A (show KDM3A Proteins)-KLF2-IRF4 (show IRF4 Proteins) pathway plays an essential role in multiple myeloma cell survival and homing to the bone marrow, and therefore represents a therapeutic target.
Expression of KLF4 (show KLF4 Proteins) in mononuclear leukocytes positively correlates with cellular markers of immune activation, whereas KLF2 expression negatively correlates with markers of subclinical atherosclerosis in this HIV-infected population.
TUG1 overexpression was induced by nuclear transcription factor SP1 (show SP1 Proteins) and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC (show FAM126A Proteins) cells by binding with PRC2 and recruiting it to KLF2 promoter region.
studies identify gain of MEKK3 sig (show MAP3K3 Proteins)nalling and KL (show KLF4 Proteins)F2/4 function as causal mechanisms for cerebral cavernous malformations pathogenesis that may be targeted to develop new CCM therapeutics
miR (show MYLIP Proteins)-92a coregulates KLF4 (show KLF4 Proteins) and KLF2 expression in arterial endothelium and contributes to phenotype heterogeneity associated with regional atherosusceptibility and protection in vivo.
Under steady-state conditions, KLF2-deficient NK cells alter their expression of homeostatic homing receptors and subsequently undergo apoptosis due to IL-15 (show IL15 Proteins) starvation.
KLF2 knockdown markedly reduced expression of miR (show MLXIP Proteins)-155 in macrophages and macrophage activation.
study therefore establishes the pivotal role of Klf2 and Tfcp2l1 (show TFCP2L1 Proteins) in mediating ESC self-renewal promoted by Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling.
endothelial-specific loss of Mekk3 (show MAP3K3 Proteins), Klf2 or Klf4 (show KLF4 Proteins) markedly prevents cerebral cavernous malformation lesion formation, reverses the increase in Rho activity, and rescues lethality
knockdown of Klf2 expression in endothelial cells induced more endothelial cell injury in early diabetic nephropathy
Cineromycin B inhibited adipocyte differentiation in 3T3-L1 cells mainly via upregulation of KLF2 and KLF3 (show KLF3 Proteins) mRNA expression at an early stage of the differentiation.
Data reveal a novel role of HDAC5 (show HDAC5 Proteins) in modulating the KLF2 transcriptional activation and eNOS (show NOS3 Proteins) expression.
inhibition of leukocyte adhesion by Myocyte enhancer factor 2 C was partially mediated by induction of KLF2
KLF2 is pivotal for coordinating CD4 (show CD4 Proteins)(+) T cell differentiation through two distinct and complementary mechanisms: via control of T cell localization and by regulation of lineage-defining transcription factors.
The Kruppel-like factor 2 (Klf2) is phosphorylated by Erk2 (show MAPK1 Proteins) and that phospho-Klf2 is proteosomally degraded.
KLF2 and ERG (show ERG Proteins) associate in a physical complex and the two proteins synergistically activate transcription of Flk1 (show KDR Proteins).
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
Kruppel-like factor 2 (lung)
, Krueppel-like factor 2
, Kruppel-like factor LKLF
, lung Kruppel-like zinc finger transcription factor
, lung krueppel-like factor
, lung Kruppel-like factor