anti-Kruppel-Like Factor 6 (KLF6) Antibodies

Human Kruppel-Like Factor 6 (KLF6) interaction partners

1. PAC-1 induces HIF1alpha stabilization and DNA damage by sequestering ferrous iron.

2. Bcd1p controls RNA loading of the core protein Nop58 during C/D box snoRNP biogenesis.

3. KLF6 knockdown partially abrogated the effects of miR18b inhibition on gastric cancer cell proliferation and invasion.

4. Study describes molecular signaling network that links the super enhancer-associated transcription factor KLF6 to lipid metabolism and enhanced mTOR activity in clear cell renal cell carcinoma.

5. blocking TGF-b signaling with the TGF-b receptor inhibitor SB431542 counteracted the effect of platelets on KLF6 expression and proliferation of HCC cells. Based on these findings, we conclude that platelet releasates, especially TGF-b, promote the proliferation of SMMC.7721 and HepG2 cells by decreasing expression of KLF6

6. mitochondrial injury and apoptosis were significantly attenuated with overexpression of KLF6 in cultured human podocytes under hyperglycemic conditions. Finally, we observed a significant reduction in glomerular and podocyte-specific expression of KLF6 in human kidney biopsies with progression of diabetic kidney disease.

7. Decreased expression of KLF6-SV2 may be associated with the occurrence and development of colorectal cancer. KLF6-SV2 plays a role as tumor suppressor by efficiently blocking cell proliferation, arresting cell cycle and inducing apoptosis in colorectal cancer, which may be related to increased expression of p21 and Bax.

8. establish a novel molecular mechanism by which miR-148a-3p upregulates Tsp-4 expression in tenocytes to promote angiogenesis by targeting KLF6, which could be helpful for the treatment of tendinopathy in the future

9. KLF6 IVS 1-27 G > A may not be associated with cancer susceptibility, especially the susceptibility of unselected prostate cancer.

10. miR-181a is up-regulated in clear cell renal cell carcinoma and may act as a tumor promoting factor by targeting KLF6 expression.

11. Overexpression of KLF6-SV1 is associated with young patients, and loss of E-cadherin suggests that this variant correlated with the aggressiveness of nasopharyngeal carcinoma.

12. Overexpression of KLF6 markedly attenuated the oncogenic effect of miR-543 overexpression in clear cell renal cell carcinoma.

13. analyzed the expression of the wild type (WT) gene KLF6 and the oncogenic splice variant 1 (KLF6-SV1) at the mRNA level in subsets of T cells from CLL patients (n = 29), multiple myeloma patients (n = 6) and normal donors (n = 10)

14. Zymography assay demonstrated that KLF6 inhibited the activities of matrix metalloproteinase 9 (MMP-9) and weakened the expression of mesenchymal markers, such as snail, slug, and vimentin. Our study is the first to provide demonstrate that KLF6 functions as a tumor suppressor gene and prevents the metastasis of oral cancer cells.

15. DJ-1 knockdown increased KLF6 expression in bortezomib-resistant myeloma cells, and subsequent siRNA-mediated KLF6 knockdown rescued bortezomib-resistant myeloma cells from undergoing cell death.

16. Our study provides new evidence that interaction of KLF6 and Sp1 regulates basigin-2 expression in hepatocellular carcinoma

17. MIIP and PAK1 bind each other and a C-terminal polyproline domain of MIIP is required for PAK1 binding. Ectopically expressed MIIP consistently competed with Rac1-GTP for binding with the PAK1 p21-binding domain in endometrial cancer cells.

18. hypoxia induced an early and transient increase in KLF6 protein levels in HTR8/SVneo extravillous cytotrophoblast cells and in placental explants. Reoxygenation returned KLF6 protein to basal levels. Moreover, hypoxia-induced up-regulation of KLF6 expression was dependent on HIF-1alpha. These results indicate that KLF6 may mediate some of the effects of hypoxia in placental development.

19. The study highlights the central role of myeloid KLF6 in promoting intestinal inflammation.

20. study identifies a new mechanism by which KLF6 regulates NF-kappaB signaling, and how this mechanism is circumvented in glioblastoma through KLF6 loss.

Mouse (Murine) Kruppel-Like Factor 6 (KLF6) interaction partners

1. KLF6 and STAT3 co-occupy regulatory DNA and functionally synergize to promote axon growth in CNS neurons

2. We observed that the loss of KLF6 in podocytes reduced the expression of synthesis of cytochrome c oxidase 2 with resultant increased mitochondrial injury, leading to activation of the intrinsic apoptotic pathway under diabetic conditions.

3. NEAT1 was significantly increased in CCl4-induced mice and activated HSCs. Loss of NEAT1 suppressed liver fibrosis in vivo and in vitro. KLF6 and miR-122 were required for the effects of NEAT1 on HSC activation. NEAT1 contributes to HSC activation via competitively binding miR-122.

4. KLF6-mediated activation of the human INSL3 promoter required an intact KLF element as well as Leydig/Sertoli-enriched factors. KLF6 transcriptionally cooperates with NUR77 and SF1. our results identify KLF6 as a regulator of human INSL3 transcription.

5. The study highlights the central role of myeloid KLF6 in promoting intestinal inflammation.

6. we identified novel transcriptional targets of KLF6 in HCC cells including VAV3, a known activator of the RAC1 small GTPase. Indeed, RAC1 activity is increased in KLF6-knockdown cells in a VAV3-dependent manner, and knockdown of either RAC1 or VAV3 impairs HCC cell migration. Together, our data demonstrate a novel function for KLF6 in constraining HCC dissemination through the regulation of a VAV3-RAC1 signaling axis.

7. Klf6 as required for developmental central nervous system myelination.Klf6 promotes oligodendrocyte differentiation and viability.

8. observations reveal that KLF6 repress BCL6 to enhance macrophage inflammatory gene expression and function.

9. present studies on the cardiac function of KLF6 show a new mechanism whereby cardiomyocytes regulate cardiac fibrosis through transcriptional control of the extracellular matrix factor thrombospondin 4

10. downregulates expression and secretion of granulocyte macrophage colony-stimulating factor

11. KLF6-dependent regulation of the cytochrome c oxidase assembly gene is critical for maintaining mitochondrial function and preventing podocyte apoptosis.

12. findings provide novel evidence highlighting KLF6 function in response to malignant transformation, suggesting the relevance of KLF6 in controlling cell proliferation and hindering tumorigenesis

13. KLF6 is required for optimal LPS-induced pro-inflammatory gene expression, acting cooperatively with NF-kappaB

14. KLF6 is a novel regulator of hepatic glucose and lipid metabolism in fatty liver.

15. ALK1 is upregulated in endothelial cells during vascular injury by a synergistic cooperative mechanism between KLF6 and specificity protein 1.

16. A direct interaction of Kruppel-like factor 6 (KLF6) with iNOS promoter is observed during in vivo flu infection of mouse respiratory tract.

17. Glucokinase links Kruppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver disease.

18. KLF6 is inducible in the hippocampus and may be associated with glial responses, especially HSP47-related tissue remodeling after pilocarpine-induced status epilepticus.

19. KLF6 deficiency contributes significantly to the carcinogenic milieu in human and murine HCC and uncover a novel tumor suppressor activity of KLF6 in HCC by linking its transcriptional repression of Mdm2 to stabilizing p53

20. copeb/Klf6 is essential for the development of endoderm-derived organs

Zebrafish Kruppel-Like Factor 6 (KLF6) interaction partners

1. Klf6a promotes hematopoietic stem and progenitor cell maintenance through Ccl25b-Ccr7 chemokine signaling.

2. In the spinal cord, klf7- and klf6a-expressing cells are found in both the dorsal and ventral horns. Numerous sensory structures (e.g. auditory, lateral line, olfactory and visual) and several motor nuclei (e.g. oculomotor, trigeminal, and vagal motor nuclei) contain klf7- and/or klf6a-expressing cells

3. copeb/Klf6 is essential for the development of endoderm-derived organs