anti-Kruppel-Like Factor 5 (Intestinal) (KLF5) Antikörper

Mouse (Murine) Kruppel-Like Factor 5 (Intestinal) (KLF5) Interaktionspartner

1. any one of Klf2 (zeige KLF2 Antikörper), Klf4 (zeige KLF4 Antikörper) and Klf5 was sufficient to support self-renewal of mouse embryonic stem cells, whereas the removal of all three compromised it.

2. the regulatory crosstalk between KLF5, miR (zeige MLXIP Antikörper)-29a, and Fbw7/CDC4 (zeige FBXW7 Antikörper) cooperatively promotes atherosclerotic development

3. KLF5 as an essential factor required for acinar-to-ductal metaplasia and oncogenic KRAS-induced pancreatic tumor formation.

4. lf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD (zeige MYOD1 Antikörper) and Mef2 (zeige MEF2C Antikörper), and Klf5 physically associates with both MyoD (zeige MYOD1 Antikörper) and Mef2 (zeige MEF2C Antikörper). In addition, MyoD (zeige MYOD1 Antikörper) 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 (zeige MYOD1 Antikörper) and Mef2 (zeige MEF2C Antikörper).

5. KLF5 regulates intestinal barrier function by mediating the transcription of DSG2 (zeige DSG2 Antikörper), a gene encoding a major component of desmosome structures

6. Klf5 suppresses Fgf4 (zeige FGF4 Antikörper)-Fgfr (zeige FGFR2 Antikörper)-ERK (zeige EPHB2 Antikörper) signalling, thus preventing precocious activation of the primitive endoderm specification programme

7. In conclusion, the results of this study suggest that the presence of KLF5 in postn (zeige POSTN Antikörper)-positive cells contributes to the pathogenesis of aortic thickening induced by DOCA-salt hypertension.

8. 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 (zeige NT5C2 Antikörper), promoting increased neutrophil output at the expense of eosinophil production.

9. Collectively, we identify a novel regulatory pathway in which 1, 25(OH)2D3 induces VDR (zeige CYP27B1 Antikörper) expression and promotes VDR (zeige CYP27B1 Antikörper) interaction with p50 subunit of NF-kappaB (zeige NFKB1 Antikörper), which in turn attenuates the association of KLF5 with p50 subunit of NF-kappaB (zeige NFKB1 Antikörper) and thus exerts anti-inflammatory and anti-proliferative effects on macrophages.

10. KLF5-dependent regulation of Myo9b (zeige MYO9B Antikörper)/RhoA (zeige RHOA Antikörper) is required for podosome formation and macrophage migration during abdominal aortic aneurysm.

Human Kruppel-Like Factor 5 (Intestinal) (KLF5) Interaktionspartner

1. 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.

2. KLF5 has a role in regulating IL1beta (zeige IL1B Antikörper) induced intervertebral disc metabolism

3. Levels of KLF5 are increased in human pancreatic ductal adenocarcinoma.

4. Data demonstrate that KLF5 inhibits ccRCC growth as a tumor suppressor and highlight the potential of 5-Aza-CdR (zeige RUNX1T1 Antikörper) to release KLF5 expression as a therapeutic modality for the treatment of ccRCC.

5. The present study found that the KLF4 (zeige KLF4 Antikörper) and KLF5 3'-UTR (zeige UTS2R Antikörper) contains one conserved target site of miR (zeige MLXIP Antikörper)-506 and miR (zeige MLXIP Antikörper)-124, and the overexpression of miR (zeige MLXIP Antikörper)-506 and miR (zeige MLXIP Antikörper)-124 inhibited the H2O2-induced upregulation of KLF4 (zeige KLF4 Antikörper) and KLF5 in HCMs.

6. miR (zeige MLXIP Antikörper)-5195-3p suppressed proliferation and invasion of human bladder cancer cells via suppression of KLF5.

7. miR (zeige MLXIP Antikörper)-217 suppresses triple-negative breast cancer cell growth, migration, and invasion. MiR (zeige MLXIP Antikörper)-217 suppresses triple-negative breast cancer, at least partially, through down-regulating the KLF5 expression.

8. 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 (zeige CCNE1 Antikörper) polymorphic intronic enhancer to confer increased bladder cancer risk.

9. demonstrate that a 186bp region is the minimal essential region and that Sp3 (zeige SP3 Antikörper)-GC1 (zeige OLFM4 Antikörper) binding is essential to the basal expression of KLF5

10. We provide the first evidence that the expression of KLF5 is up-regulated in small airways and pulmonary vessels of patients with COPD (zeige ARCN1 Antikörper) and may be involved in the tissue remodeling of COPD (zeige ARCN1 Antikörper).