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

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

1. These results indicate that Klf5 plays a critical role in the ductular reaction and biliary epithelial tissue expansion and remodeling by inducing biliary epithelial cell proliferation and thereby contributing to liver regeneration.

2. any one of Klf2, Klf4 and Klf5 was sufficient to support self-renewal of mouse embryonic stem cells, whereas the removal of all three compromised it.

3. the regulatory crosstalk between KLF5, miR-29a, and Fbw7/CDC4 cooperatively promotes atherosclerotic development

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

5. lf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD and Mef2, and Klf5 physically associates with both MyoD and Mef2. In addition, MyoD 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 and Mef2.

6. KLF5 regulates intestinal barrier function by mediating the transcription of DSG2, a gene encoding a major component of desmosome structures

7. Klf5 suppresses Fgf4-Fgfr-ERK signalling, thus preventing precocious activation of the primitive endoderm specification programme

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

9. 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, promoting increased neutrophil output at the expense of eosinophil production.

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

11. KLF5-dependent regulation of Myo9b/RhoA is required for podosome formation and macrophage migration during abdominal aortic aneurysm.

12. 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).

13. 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

14. Cardiac myocyte KLF5 is a transcriptional regulator of Ppara and cardiac energetics.

15. In embryonic stem cells, we show that Klf5, but not JunB is a key LIF effector of cell plasticity.

16. the regulatory functions of Klf5 acetylation in ESC self-renewal and differentiation

17. unravels a novel mechanism how matrix stiffness regulates cellular proliferation and highlights the importance of matrix stiffness-modulated Klf5/Klf4 in the regulation of renal physiologic functions and fibrosis progression

18. that estrogen biphasically modulates prostate tumor formation by regulating Kruppel-like zinc finger transcription factor 5-dependent transcription through estrogen receptor beta

19. KLF5 loss enhances tumor angiogenesis by attenuating PI3K/AKT signaling and subsequent accumulation of HIF1alpha in PTEN deficient prostate tumors.

20. Simultaneous downregulation of KLF5 and Fli1 is a key feature underlying systemic sclerosis.

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

1. These results revealed that KLF5 promotes the tumorigenesis and metastasis of thyroid cancer cells and may be a potential therapeutic target in patients with thyroid cancer

2. the present findings were the first to show that KLF5 expression and nitration by iNOS-mediated peroxynitrite are necessary for the induction of TNF-alpha and IL-1beta expression in VSMCs of diabetic vascular tissues.

3. 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.

4. 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.

5. correlation between the KLF5 and ZEB1 transcription levels in the pancreatic tumor tissues

6. The present study has identified that KLF5, a target of miR-145-5p, is a key marker gene in cancer. miR-145-5p may also contribute to the dysregulation of other functional genes during tumor development.

7. the knockdown of HDAC1/2 upregulated KLF5 protein but not KLF5 mRNA, and the increase in KLF5 protein level by silencing HDAC1/2 was at least in part due to decreased proteasomal degradation.

8. 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.

9. KLF5 has a role in regulating IL1beta induced intervertebral disc metabolism

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

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

12. The present study found that the KLF4 and KLF5 3'-UTR contains one conserved target site of miR-506 and miR-124, and the overexpression of miR-506 and miR-124 inhibited the H2O2-induced upregulation of KLF4 and KLF5 in HCMs.

13. miR-5195-3p suppressed proliferation and invasion of human bladder cancer cells via suppression of KLF5.

14. miR-217 suppresses triple-negative breast cancer cell growth, migration, and invasion. MiR-217 suppresses triple-negative breast cancer, at least partially, through down-regulating the KLF5 expression.

15. 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 polymorphic intronic enhancer to confer increased bladder cancer risk.

16. demonstrate that a 186bp region is the minimal essential region and that Sp3-GC1 binding is essential to the basal expression of KLF5

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

18. our results indicate that KLF5 promotes angiogenesis of bladder cancer through directly regulating VEGFA transcription

19. Data indicate direct binding of microRNA miR-375 to the 3'-untranslated region of transcription factor KLF5.

20. findings collectively suggest that TNFAIP2 is a direct KLF5 target gene, and both KLF5 and TNFAIP2 promote breast cancer cell proliferation, migration and invasion through Rac1 and Cdc42