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KLF5 encodes a member of the Kruppel-like factor subfamily of zinc finger proteins. Additionally we are shipping KLF5 Antibodies (77) and KLF5 Kits (9) and many more products for this protein.
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any one of Klf2 (show KLF2 Proteins), Klf4 (show KLF4 Proteins) and Klf5 was sufficient to support self-renewal of mouse embryonic stem cells, whereas the removal of all three compromised it.
the regulatory crosstalk between KLF5, miR (show MLXIP Proteins)-29a, and Fbw7/CDC4 (show FBXW7 Proteins) cooperatively promotes atherosclerotic development
KLF5 as an essential factor required for acinar-to-ductal metaplasia and oncogenic KRAS-induced pancreatic tumor formation.
lf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD (show MYOD1 Proteins) and Mef2 (show MEF2C Proteins), and Klf5 physically associates with both MyoD (show MYOD1 Proteins) and Mef2 (show MEF2C Proteins). In addition, MyoD (show MYOD1 Proteins) 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 Proteins) and Mef2 (show MEF2C Proteins).
KLF5 regulates intestinal barrier function by mediating the transcription of DSG2 (show DSG2 Proteins), a gene encoding a major component of desmosome structures
Klf5 suppresses Fgf4 (show FGF4 Proteins)-Fgfr (show FGFR2 Proteins)-ERK (show EPHB2 Proteins) 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 Proteins)-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 Proteins), 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 Proteins) expression and promotes VDR (show CYP27B1 Proteins) interaction with p50 subunit of NF-kappaB (show NFKB1 Proteins), which in turn attenuates the association of KLF5 with p50 subunit of NF-kappaB (show NFKB1 Proteins) and thus exerts anti-inflammatory and anti-proliferative effects on macrophages.
KLF5-dependent regulation of Myo9b/RhoA (show RHOA Proteins) is required for podosome formation and macrophage migration during abdominal aortic aneurysm.
the results of the present study suggested that the miR5905p/KLF5 axis may regulate osteosarcoma (OS)progression and thus, may be a novel therapeutic target for the treatment of patients with OS.
Study showed that KLF5 expression was increased in intracranial aneurysms (IAs) patients compared to that of normal subjects, and KLF5 overexpression vascular smooth muscle cells proliferation, migration, and phenotypic modulation, suggesting that the upregulated KLF5 expression played an important role in the induction of IAs.
correlation between the KLF5 and ZEB1 transcription levels in the pancreatic tumor tissues
The present study has identified that KLF5, a target of miR (show MLXIP Proteins)-145-5p, is a key marker gene in cancer. miR (show MLXIP Proteins)-145-5p may also contribute to the dysregulation of other functional genes during tumor development.
the knockdown of HDAC1 (show HDAC1 Proteins)/2 upregulated KLF5 protein but not KLF5 mRNA, and the increase in KLF5 protein level by silencing HDAC1 (show HDAC1 Proteins)/2 was at least in part due to decreased proteasomal degradation.
KLF5 expression in tumor stroma was closely associated with clinicopathological features such as tumor size, invasion depth, cell grade and lymph node metastasis, as well as poor prognosis in patients with gastric cancer.
KLF5 has a role in regulating IL1beta (show IL1B Proteins) induced intervertebral disc metabolism
Levels of KLF5 are increased in human pancreatic ductal adenocarcinoma.
Data demonstrate that KLF5 inhibits ccRCC growth as a tumor suppressor and highlight the potential of 5-Aza-CdR (show RUNX1T1 Proteins) to release KLF5 expression as a therapeutic modality for the treatment of ccRCC.
The present study found that the KLF4 (show KLF4 Proteins) and KLF5 3'-UTR contains one conserved target site of miR (show MLXIP Proteins)-506 and miR (show MLXIP Proteins)-124, and the overexpression of miR (show MLXIP Proteins)-506 and miR (show MLXIP Proteins)-124 inhibited the H2O2-induced upregulation of KLF4 (show KLF4 Proteins) and KLF5 in HCMs.
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