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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 5

KLF5, BTEB2, Kruppel-like factor 5, IKLF
This gene encodes a member of the Kruppel-like factor subfamily of zinc finger proteins. Since the protein localizes to the nucleus and binds the epidermal growth factor response element, it is thought to be a transcription factor. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: KLF4, CAN, V1a, PCNA, ACID
Papers using KLF5 antibodies
Papers on KLF5
KLF5 promotes cell migration by up-regulating FYN in bladder cancer cells.
Guo et al., Xi'an, China. In Febs Lett, Feb 2016
UNASSIGNED: KLF5 promotes cell proliferation of bladder cancer.
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.
Dissection of transcriptional and cis-regulatory control of differentiation in human pancreatic cancer.
Natoli et al., Milano, Italy. In Embo J, Feb 2016
Among the candidate regulators of PDAC differentiation, KLF5 was selectively expressed in pre-neoplastic lesions and low-grade primary PDACs and cell lines, where it maintained the acetylation of grade-specific enhancers, the expression of epithelial genes such as keratins and mucins, and the ability to organize glandular epithelia in xenografts.
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.
Recent advances in animal models of systemic sclerosis.
Asano, Tokyo, Japan. In J Dermatol, Jan 2016
Under this situation, three new genetic animal models have recently been established, such as Fra2 transgenic mice, urokinase-type plasminogen activator receptor deficient mice and Klf5(+/-) ;Fli1(+/-) mice, all of which recapitulate the pathological cascade of SSc.
Identification of focally amplified lineage-specific super-enhancers in human epithelial cancers.
Meyerson et al., Boston, United States. In Nat Genet, Jan 2016
Copy number gains of noncoding regions harboring super-enhancers near KLF5, USP12, PARD6B and MYC are associated with overexpression of these cancer-related genes.
Murine Embryonic Stem Cell Plasticity Is Regulated through Klf5 and Maintained by Metalloproteinase MMP1 and Hypoxia.
Boeuf et al., Bordeaux, France. In Plos One, Dec 2015
By employing a LIF-dependent 'plasticity' test, that we set up, we show that Klf5, but not JunB is a key LIF effector.
Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds.
Shin et al., Atlanta, United States. In Semin Cancer Biol, Dec 2015
Here, we define the anti-growth signaling process, and review several important pathways involved in growth signaling: p53, phosphatase and tensin homolog (PTEN), retinoblastoma protein (Rb), Hippo, growth differentiation factor 15 (GDF15), AT-rich interactive domain 1A (ARID1A), Notch, insulin-like growth factor (IGF), and Krüppel-like factor 5 (KLF5) pathways.
Vasculopathy in scleroderma.
Sato et al., Tokyo, Japan. In Semin Immunopathol, Sep 2015
Recent new insights into the therapeutic mechanisms of intravenous cyclophosphamide pulse and bosentan and the establishment of a new SSc animal model (Klf5 (+/-);Fli1 (+/-) mice) provide us useful clues to further understand the development of vascular alterations characteristic of SSc.
Double heterozygous mice for Klf5 and Fli1 genes: a new animal model of systemic sclerosis recapitulating its three cardinal pathological features.
Asano, Tokyo, Japan. In Med Mol Morphol, Sep 2015
This notion is supported by the establishment of a new murine SSc model which recapitulates three cardinal features of SSc by simultaneous haploinsufficiency of Klf5 and Fli1 genes, both of which are epigenetically suppressed in SSc dermal fibroblasts.
Common variation at 2p13.3, 3q29, 7p13 and 17q25.1 associated with susceptibility to pancreatic cancer.
Klein et al., Baltimore, United States. In Nat Genet, Aug 2015
We replicated previously reported associations at 9q34.2 (ABO), 13q22.1 (KLF5), 5p15.33 (TERT and CLPTM1), 13q12.2
C/EBPα in normal and malignant myelopoiesis.
Friedman, Baltimore, United States. In Int J Hematol, Apr 2015
C/EBPα interacts with AP-1 proteins to bind hybrid DNA elements during monopoiesis, and induction of Gfi-1, C/EBPε, KLF5, and miR-223 by C/EBPα enables granulopoiesis.
Genome-wide profiling of HPV integration in cervical cancer identifies clustered genomic hot spots and a potential microhomology-mediated integration mechanism.
Ma et al., Wuhan, China. In Nat Genet, Feb 2015
Beyond recalculating frequencies for the previously reported frequent integration sites POU5F1B (9.7%), FHIT (8.7%), KLF12 (7.8%), KLF5 (6.8%), LRP1B (5.8%) and LEPREL1 (4.9%), we discovered new hot spots HMGA2 (7.8%), DLG2 (4.9%) and SEMA3D (4.9%).
KLF5 and hhLIM cooperatively promote proliferation of vascular smooth muscle cells.
Zheng et al., Shijiazhuang, China. In Mol Cell Biochem, 2012
KLF5 reverses hhLIM function from anti-proliferation to pro-proliferation through its interaction with hhLIM on the cyclin E promoter.
O-GlcNAc regulates pluripotency and reprogramming by directly acting on core components of the pluripotency network.
Youn et al., Seoul, South Korea. In Cell Stem Cell, 2012
O-GlcNAc modification of threonine 228 in Oct4 regulates Oct4 transcriptional activity and is important for inducing many pluripotency-related genes, including Klf2, Klf5, Nr5a2, Tbx3, and Tcl1.
Krüppel-like zinc-finger transcription factor 5 (KLF5) is highly expressed in large and giant unruptured cerebral aneurysms.
Satoh et al., Tokushima, Japan. In World Neurosurg, 2012
KLF5 is highly expressed in large and giant unruptured aneurysms and that in ruptured aneurysmal wall KLF5 expression was scarce.
Kruppel-like factor 5 (KLF5) is critical for conferring uterine receptivity to implantation.
Dey et al., Cincinnati, United States. In Proc Natl Acad Sci U S A, 2012
Klf5 is indispensable for normal blastocyst implantation in the uterus.
Krüppel-like factor 5 protects against murine colitis and activates JAK-STAT signaling in vivo.
Katz et al., Philadelphia, United States. In Plos One, 2011
we have used a novel transgenic mouse model to demonstrate an essential role for KLF5 in intestinal epithelial homeostasis and in mucosal healing following induction of experimental colitis.
Regulatory role of Klf5 in early mouse development and in embryonic stem cells.
Russo et al., Napoli, Italy. In Vitam Horm, 2010
Data suggest that Klf5 activates expression of self-renewal-promoting genes and inhibits expression of differentiation-related genes embryonic stem cells. [REVIEW]
Krüppel-like factor 5 is essential for blastocyst development and the normal self-renewal of mouse ESCs.
Fujii-Kuriyama et al., Tsukuba, Japan. In Cell Stem Cell, 2008
essential for blastocyst development and the normal self-renewal of mouse ESCs
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