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Kruppel-like factors (KLFs) are a family of broadly expressed zinc finger transcription factors. Additionally we are shipping KLF2 Antibodies (111) and KLF2 Kits (11) and many more products for this protein.
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Authors found that there was negative correlation between LINC01133 and KLF2, P21 (show CDKN1A Proteins) or E-cadherin (show CDH1 Proteins) in NSCLC.
Authors found that knockdown of ANRIL expression could impair cell proliferation and invasion and induce cell apoptosis both in vitro and in vivo. Authors also found that ANRIL could epigenetically repress KLF2 transcription in HCC (show FAM126A Proteins) cells by binding with PRC2 and recruiting it to KLF2 promoter region.
KLF2 and KLF4 (show KLF4 Proteins) serve as important regulators that promote hemoglobin alpha (show HBA1 Proteins) expression in the endothelium.
Upregulated long non-coding RNA AGAP2 (show AGAP2 Proteins)-AS1 (show PTGDR Proteins) represses LATS2 and KLF2 expression through interacting with EZH2 (show EZH2 Proteins) and LSD1 (show KDM1A Proteins) in non-small-cell lung cancer cells.
Transcription factor Kruppel-like factor 2 (KLF2) of the zinc finger family of DNA-binding proteins has recently emerged as a major molecular switch that controls endothelial homeostasis.
The findings point to KLF2 as a new gene involved in heritable pulmonary arterial hypertension.
we provide evidence that the tumor-suppressive microRNA miR (show MLXIP Proteins)-1825 controls KLF2 expression. Reporter gene analyses revealed that both microRNAs directly targeted the 3'-untranslated region of KLF2 messenger RNA. These data demonstrated that miR (show MLXIP Proteins)-1825 expression in serum of human glioma was associated with tumorigenesis and miR (show MLXIP Proteins)-1825 may be used as a biomarker for identification of the pathological grade of glioma.
Long noncoding RNA XIST acts as an oncogene (show RAB1A Proteins) in non-small cell lung cancer by epigenetically repressing KLF2 expression.
lysine-specific demethylase (show MBD2 Proteins)-1 is an important oncogene (show RAB1A Proteins) in gastric cancer, and lysine-specific demethylase (show MBD2 Proteins)-1-mediated epigenetic repression of KLF2 plays a critical role in gastric cancer development and progression.
KLF2 is shown to be downregulated in pancreatic ductal adenocarcinoma (PDAC) clinical samples and overexpression of KLF2 inhibits the growth, migration, and metastasis of PDAC cancer cells.
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.
KLF2 and KLF4 (show KLF4 Proteins) serve as important regulators that promote hemoglobin alpha (show HBA-A1 Proteins) expression in the endothelium.
Mouse embryos deficient in Orai1 (show TMEM132A Proteins), Klf2, or Klf4 (show KLF4 Proteins) showed a significantly reduced lymphatic density and impaired lymphatic development.
this study shows that KLF2 governs the degree of dendritic cells activation and hence the intensity of proatherogenic T cell responses
A deficiency of KLF2 increased the expression of Notch ligand (show JAG2 Proteins) Jagged2 (show JAG2 Proteins) via hypoxia-inducible factor 1alpha (HIF-1alpha (show HIF1A Proteins)), which led to Th2 amplification.
our data demonstrate a protective role of KLF2 against glomerular endothelial cell injury and progression of chronic kidney disease in the model of compensatory renal hypertrophy
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
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