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KLF5 encodes a member of the Kruppel-like factor subfamily of zinc finger proteins. Additionally we are shipping KLF5 Antibodies (69) and KLF5 Proteins (5) and many more products for this protein.
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lf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD (show MYOD1 ELISA Kits) and Mef2 (show MEF2C ELISA Kits), and Klf5 physically associates with both MyoD (show MYOD1 ELISA Kits) and Mef2 (show MEF2C ELISA Kits). In addition, MyoD (show MYOD1 ELISA Kits) recruitment was greatly reduced in the absence of Klf5. These results indicate that Klf5 is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD (show MYOD1 ELISA Kits) and Mef2 (show MEF2C ELISA Kits).
KLF5 regulates intestinal barrier function by mediating the transcription of DSG2 (show DSG2 ELISA Kits), a gene encoding a major component of desmosome structures
Klf5 suppresses Fgf4 (show FGF4 ELISA Kits)-Fgfr (show FGFR2 ELISA Kits)-ERK (show EPHB2 ELISA Kits) signalling, thus preventing precocious activation of the primitive endoderm specification programme
In conclusion, the results of this study suggest that the presence of KLF5 in postn (show POSTN ELISA Kits)-positive cells contributes to the pathogenesis of aortic thickening induced by DOCA-salt hypertension.
these studies demonstrate dual functions of Klf5 in regulating hematopoietic stem and progenitor proliferation and localization in the bone marrow, as well as lineage choice after GMP (show NT5C2 ELISA Kits), promoting increased neutrophil output at the expense of eosinophil production.
Collectively, we identify a novel regulatory pathway in which 1, 25(OH)2D3 induces VDR (show CYP27B1 ELISA Kits) expression and promotes VDR (show CYP27B1 ELISA Kits) interaction with p50 subunit of NF-kappaB (show NFKB1 ELISA Kits), which in turn attenuates the association of KLF5 with p50 subunit of NF-kappaB (show NFKB1 ELISA Kits) and thus exerts anti-inflammatory and anti-proliferative effects on macrophages.
KLF5-dependent regulation of Myo9b/RhoA (show RHOA ELISA Kits) is required for podosome formation and macrophage migration during abdominal aortic aneurysm.
Data show that R-Smad Proteins SMAD1 and SMAD5, which transduce bone morphogenetic protein (BMP) signals, recognize enhancer regions together with Kruppel-like factors KLF4 and KLF5 in naive embryonic stem cell (mESCs).
illustrates that KLF5 may modulate DNA repair pathways to prevent intestinal injury induced by TBI. KLF5 signaling provides a novel field for identification of potential therapeutic targets for the treatment of radiation-induced intestinal damage
Cardiac myocyte KLF5 is a transcriptional regulator of Ppara (show PPARA ELISA Kits) and cardiac energetics.
miR (show MLXIP ELISA Kits)-217 suppresses triple-negative breast cancer cell growth, migration, and invasion. MiR (show MLXIP ELISA Kits)-217 suppresses triple-negative breast cancer, at least partially, through down-regulating the KLF5 expression.
Data reveal that the presence of rs200996365, a SNP in high-linkage disequilibrium with rs8102137 residing in the center of a KLF5 motif, alters KLF5 binding to this genomic region and provide evidence that KLF5 binds CCNE1 (show CCNE1 ELISA Kits) polymorphic intronic enhancer to confer increased bladder cancer risk.
demonstrate that a 186bp region is the minimal essential region and that Sp3 (show SP3 ELISA Kits)-GC1 (show OLFM4 ELISA Kits) binding is essential to the basal expression of KLF5
We provide the first evidence that the expression of KLF5 is up-regulated in small airways and pulmonary vessels of patients with COPD (show ARCN1 ELISA Kits) and may be involved in the tissue remodeling of COPD (show ARCN1 ELISA Kits).
our results indicate that KLF5 promotes angiogenesis of bladder cancer through directly regulating VEGFA (show VEGFA ELISA Kits) transcription
Data indicate direct binding of microRNA miR (show MLXIP ELISA Kits)-375 to the 3'-untranslated region of transcription factor KLF5.
findings collectively suggest that TNFAIP2 (show TNFAIP2 ELISA Kits) is a direct KLF5 target gene, and both KLF5 and TNFAIP2 (show TNFAIP2 ELISA Kits) promote breast cancer cell proliferation, migration and invasion through Rac1 and Cdc42 (show CDC42 ELISA Kits)
ABL-N administration induced apoptosis of PC3 cells in a dose-dependent manner, along with the enhanced activity of caspases and increased Bax/Bcl-2 ratio. Expression of KLF5, Stat5b and ICAM-1 was significantly downregulated in PC3 cells.
KLF5/Sox4 regulatory signaling play an important role in lung tumorigenesis, which might represent novel therapeutic targets to manage lung carcinoma.
BAP1 (show RNF2 ELISA Kits) interacts directly with KLF5 and stabilizes KLF5 via deubiquitination.
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.
Kruppel-like factor 5 (intestinal)
, Krueppel-like factor 5-like
, Kruppel-like factor 5
, basic-transcription-element-binding-protein 2
, basic transcription element binding protein 2
, basic transcription element binding protein BTEB2
, BTE-binding protein 2
, Krueppel-like factor 5
, basic transcription element-binding protein 2
, intestinal-enriched krueppel-like factor
, transcription factor BTEB2
, GC box binding protein 2
, GC-box-binding protein 2
, colon krueppel-like factor
, colon kruppel-like factor
, intestinal-enriched kruppel-like factor