Kruppel-Like Factor 11 (KLF11) ELISA Kits

Human Kruppel-Like Factor 11 (KLF11) interaction partners

1. Profibrotic gene expression was activated in a primary human peritoneal cell line in response to KLF11 short hairpin RNA and medroxyprogesterone acetate but not estradiol.

2. In endometrial-stromal fibroblasts, KLF11 recruited SIN3A/HDAC (histone deacetylase), resulting in COL1A1-promoter deacetylation and repression

3. Results suggest a role for KLF11 in upregulating MAO-A in depressive disorder and chronic social stress, suggesting that inhibition of the pathways regulated by this transcription factor may aid in the therapeutics of neuropsychiatric illnesses

4. The data suggest a relationship between promoter DNA methylation and KLF11 gene expression in ovarian cancer tumorigenesis.

5. identified an evolutionarily conserved metabolic regulator, Kruppel-like factor 11 (KLF11), as a novel browning transcription factor in human adipocytes that is required for rosiglitazone-induced browning.

6. KLF11 repressed most endometrial CYP enzymes

7. Levels of KLF11 are significantly increased in the postmortem prefrontal cortex of subjects with alcohol dependence compared to controls.

8. KLF11 regulates distinct gene networks.

9. KLF111 represses glycodelin-A levels and influences its role in the ovarian endometrium.

10. KLF11 is a critical transcription factor in the function of mesenchymal cells and, specifically, as a negative regulator of collagen secretion.

11. Data identify a novel pathogenic role for KLF11 in preventing de novo disease-associated fibrosis in endometriosis.

12. The A347S mutation disrupted KLF11-mediated increases in basal insulin levels and promoter activity and blunted glucose-stimulated insulin secretion.

13. Data indicate that median methylation levels of BCAN, HOXD1, KCTD8, KLF11, NXPH1, POU4F1, SIM1, and TCF7L1 were >/=30% higher than in normal samples, representing potential biomarkers for tumor diagnosis.

14. KLF11 has a role in fine-tuning insulin transcription in certain cellular situations rather than representing a major transcriptional activator or repressor of the insulin gene.

15. Kruppel-like factor-11, a transcription factor involved in diabetes mellitus, suppresses endothelial cell activation via the nuclear factor-kappaB signaling pathway.

16. KLF11 is an MAO A regulator and is produced in response to neuronal stress, which transcriptionally activates MAO A.

17. Here we report the characterization of two antagonistic, chromatin-mediated mechanisms by which KLF11 regulated the transcription of the dopamine D2 receptor.

18. A PXVXL HP1-interacting domain identified at position 487-491 of KLF11 mediates the binding of HP1alpha and KLF11 in vitro and in cultured cells.

19. an important role for KLF11 in the regulation of INS transcription via the novel c.-331 KLF site.

20. KLF11, but not KLF15, was essential for UCP1 expression during brown adipocyte differentiation of muBM3.1.

Mouse (Murine) Kruppel-Like Factor 11 (KLF11) interaction partners

1. KLF11 acts as a novel protective factor in ischemic stroke.

2. Consistent with loss of Klf11-mediated activation, lesions in Klf11-/- animals were associated with progressive fibrosis and decreased Drd2 expression.

3. Using a sterile peritonitis model, fibrosis selectively developed in Klf11-/- females. Fibrosis in these animals was almost completely abrogated by ovariectomy. Ovariectomized animals were selectively supplemented with estradiol, medroxyprogesterone acetate (MPA), or dihydrotestosterone; fibrosis was only observed in mice exposed to MPA.

4. TGFbeta and KLF11 mediate critical, translationally relevant host and lesion-driven responses that enable establishment and progression of endometriosis.

5. Results suggest a role for KLF11 in upregulating MAO-A in depressive disorder and chronic social stress, suggesting that inhibition of the pathways regulated by this transcription factor may aid in the therapeutics of neuropsychiatric illnesses

6. Data show that the major phenotype given by the whole-body deletion of Kruppel-like factor 11 (Klf11) is not diabetes but increased insulin sensitivity.

7. Loss of KLF11 expression is associated with hyperglycemia in Type 2 diabetes.

8. this study revealed a new role for the KLF11 gene in the mechanisms underlying the antinociceptive effects of chronic ethanol exposure

9. KLF11 is a critical transcription factor in the function of mesenchymal cells and, specifically, as a negative regulator of collagen secretion.

10. Taken together, our findings identify a novel anti-hypertrophic and anti-fibrotic role of KLF11, and KLF11 activator may serve as candidate drug for heart failure patients.

11. Overexpression of KLF11 in the livers of diabetic and obese mice activates the PPARalpha signaling pathway, subsequently markedly improving the fatty liver phenotype. Knockdown of KLF11 increases hepatic triglycerides.

12. Data identify a novel pathogenic role for KLF11 in preventing de novo disease-associated fibrosis in endometriosis.

13. Recruitment of KLF11 as a novel co-regulator (with peroxisome proliferator-activated receptor PPARgamma) plays a critical role in cerebrovascular protection after ischemic insults.

14. Kruppel-like factor-11, a transcription factor involved in diabetes mellitus, suppresses endothelial cell activation via the nuclear factor-kappaB signaling pathway.

15. KLF11 is an MAO A regulator and is produced in response to neuronal stress, which transcriptionally activates MAO A.

16. an important role for KLF11 in the regulation of INS transcription via the novel c.-331 KLF site.

17. the expression of TIEG1 and TIEG2 was specific in different organs yet varied with different developmental time points.

18. KLF11 is downregulated in human cancers, inhibits cell growth in vitro and in vivo, and suppresses neoplastic transformation

19. results from genetic knockout suggest that KLF11 is not absolutely required for hematopoiesis, growth, and development

20. Tieg3/Klf11 is a downstream mediator of TGF-beta-induced apoptosis in the oligodendroglial cell line OLI-neu by transcriptional repression of Smad7