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Kruppel-like factor 4

KLF4, GKLF, Kruppel-like factor 4
a transcription factor that works with Sp1 to activate the Laminin gamma1 chain gene [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Sox2, c-Myc, CAN, Nanog, V1a
Papers using KLF4 antibodies
Induced pluripotent stem cell lines derived from human somatic cells
Kasahara Noriyuki et al., In Molecular Therapy. Nucleic Acids, 2006
... Primary antibodies used were GKLF (sc-20691; Santa Cruz Biotechnology, Santa Cruz, CA) and ...
Regulation of TRAIL expression by the phosphatidylinositol 3-kinase/Akt/GSK-3 pathway in human colon cancer cells.
Hotchin Neil A., In PLoS ONE, 2001
... KLF4 knockout in KLF4/CreER (+/−)/KLF4 (flox/flox) double transgenic mice was induced by ...
Papers on KLF4
BMP Sustains Embryonic Stem Cell Self-Renewal through Distinct Functions of Different Krüppel-like Factors.
Miyazono et al., Uppsala, Sweden. In Stem Cell Reports, Feb 2016
SMAD1 and SMAD5, which transduce BMP signals, recognize enhancer regions together with KLF4 and KLF5 in naive mESCs.
p21 and CK2 interaction-mediated HDAC2 phosphorylation modulates KLF4 acetylation to regulate bladder cancer cell proliferation.
Zhang et al., Beijing, China. In Tumour Biol, Feb 2016
UNASSIGNED: Krüppel-like factor 4 (KLF4) is a transcription factor involved in both tumor suppression and oncogenesis as a transcriptional activator or repressor in a context-dependent manner.
Enhanced OCT4 transcriptional activity substitutes for exogenous SOX2 in cellular reprogramming.
Tapia et al., Münster, Germany. In Sci Rep, Dec 2015
In this report, we show that E1A can generate iPSCs in combination with OCT4 and KLF4, thus replacing exogenous SOX2.
Generation of Arbas Cashmere Goat Induced Pluripotent Stem Cells Through Fibroblast Reprogramming.
Liu et al., Hohhot, China. In Cell Reprogram, Aug 2015
We transferred OCT4, SOX2, c-MYC, and KLF4 into Arbas cashmere goat fetal fibroblasts, then induced and cultured them using a drug-inducible system to obtain Arbas goat iPSCs that morphologically resembled mouse iPSCs.
A Unique Gene Regulatory Network Resets the Human Germline Epigenome for Development.
Surani et al., Cambridge, United Kingdom. In Cell, Jul 2015
We show that the transcriptional program of hPGCs is distinct from that in mice, with co-expression of somatic specifiers and naive pluripotency genes TFCP2L1 and KLF4.
KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis.
Owens et al., Charlottesville, United States. In Nat Med, Jun 2015
SMC-specific conditional knockout of Krüppel-like factor 4 (Klf4) resulted in reduced numbers of SMC-derived MSC- and macrophage-like cells, a marked reduction in lesion size, and increases in multiple indices of plaque stability, including an increase in fibrous cap thickness as compared to wild-type controls.
Krüppel-ling of IRF4-Dependent DCs into Two Functionally Distinct DC Subsets.
Heath et al., Melbourne, Australia. In Immunity, Jun 2015
In this issue of Immunity, Tussiwand et al. (2015) demonstrate that a dependence on KLF4 identifies a subset of IRF4-dependent DC that preferentially promotes Th2 cell differentiation.
Klf4 expression in conventional dendritic cells is required for T helper 2 cell responses.
Murphy et al., Saint Louis, United States. In Immunity, Jun 2015
Here, we have provided evidence that Kruppel-like factor 4 (Klf4) is required in IRF4-expressing cDCs to promote Th2, but not Th17, cell responses in vivo.
Genetic/molecular alterations of meningiomas and the signaling pathways targeted.
Tabernero et al., Coimbra, Portugal. In Oncotarget, Jun 2015
Thus, monosomy 22, which is often associated with mutations of the NF2 gene, has emerged as the most frequent alteration of meningiomas; in addition, several other genes (e.g., AKT1, KLF4, TRAF7, SMO) and chromosomes have been found to be recurrently altered often in association with more complex karyotypes and involvement of multiple signaling pathways.
Krüppel-like factors in hepatocellular carcinoma.
Ma et al., Shanghai, China. In Tumour Biol, Feb 2015
To date, five members (KLF4, KLF6, KLF8, KLF9, and KLF17) in the KLF family have been reported to function in the pathogenesis of HCC in multiple ways, which hold the potential of deepening and widening our understanding in the initiation and progression of HCC.
Markers of Pluripotency in Human Amniotic Epithelial Cells and Their Differentiation to Progenitor of Cortical Neurons.
Díaz et al., Ciudad López Mateos, Mexico. In Plos One, 2014
We analyzed qualitatively and quantitatively the expression of the transcription factors of pluripotency (OCT4, SOX2, NANOG, KLF4 and REX1) by RT-PCR and RT-qPCR in hAEC.
Emerging roles of Krüppel-like factor 4 in cancer and cancer stem cells.
Wang et al., China. In Asian Pac J Cancer Prev, 2014
Recent progress has highlighted the significance of KLFs, especially KLF4, in cancer and CSCs.
Different pathways of macrophage activation and polarization.
Myśliwska et al., Gdańsk, Poland. In Postepy Hig Med Dosw (online), 2014
Mediators of M1 macrophage TLR-dependent polarization include transcription factors such as NF-κB, AP-1, PU.1, CCAAT/enhancer-binding protein α (C/EBP-α), STAT1 as well as interferon regulatory factor 5 (IRF5), while the transcription factors which promote M2 activation include IRF4, C/EBP-β, Krüppel-like factor 4 (KLF4), STAT6 and PPARγ receptor.
The Role of Krüppel-like Factor 4 in Renal Fibrosis.
Fang et al., Nanchang, China. In Front Physiol, 2014
KLF4 is the most extensively studied factor among the various members of the Krüppel-like factor (KLF) family of zinc finger-containing transcription factors.
Transcriptional pause release is a rate-limiting step for somatic cell reprogramming.
Esteban et al., Guangzhou, China. In Cell Stem Cell, 2014
We further demonstrate that the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters.
Oncosecretomics coupled to bioenergetics identifies α-amino adipic acid, isoleucine and GABA as potential biomarkers of cancer: Differential expression of c-Myc, Oct1 and KLF4 coordinates metabolic changes.
Nagrath et al., United States. In Biochim Biophys Acta, 2012
Our findings establish the impact of Oct1, KLF4 and c-Myc on cancer bioenergetics and evidence a link between oncosecretomics and cellular bioenergetics profile.
KLF4 and SOX9 transcription factors antagonize β-catenin and inhibit TCF-activity in cancer cells.
Lincoln et al., Mobile, United States. In Biochim Biophys Acta, 2012
Both Sox9 and KLF4 interact with beta-catenin in an immunoprecipitation assay and reduce its binding to TCF4.
Dysregulated Krüppel-like factor 4 and vitamin D receptor signaling contribute to progression of hepatocellular carcinoma.
Xie et al., Shanghai, China. In Gastroenterology, 2012
KLF4 binds to the promoter of VDR to regulate its expression altering signal transduction and contributing to the progression of hepatocellular carcinoma.
Kruppel-like factor 4 contributes to high phosphate-induced phenotypic switching of vascular smooth muscle cells into osteogenic cells.
Hayashi et al., Tokyo, Japan. In J Biol Chem, 2012
Klf4 mediates high phosphate-induced conversion of smooth muscle cells into osteogenic cells.
Deficiency of the Kruppel-like factor KLF4 correlates with increased cell proliferation and enhanced skin tumorigenesis.
Ai et al., Columbia, United States. In Carcinogenesis, 2012
data suggest that KLF4 inhibits cell proliferation, migration and adhesion and that loss of KLF4 promotes skin tumorigenesis
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