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Human Transforming Growth Factor beta 1 Induced Transcript 1 (TGFB1I1) interaction partners

1. this paper shows that IL-17-driven intestinal fibrosis is inhibited by Itch-mediated ubiquitination of HIC-5

2. Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5.

3. Isolated Hic-5(-/-);PyMT CAFs were defective in stress fiber organization and exhibited reduced contractility. These cells also failed to efficiently deposit and organize the ECM in two and three dimensions. This, in turn, impacted three-dimensional MDA-MB-231 tumor cell migration behavior

4. Hic-5 regulates GR binding site selection by a novel mechanism, exploiting gene-specific requirements for chromatin remodeling enzymes to selectively influence DNA occupancy and gene regulation by a transcription factor.

5. As aging increased, more ARA55 were expressed in PZ stromal cells, leading to more sensitive androgen/androgen receptor (AR) signal pathway, then constituting a more feasible environment to cancer cells.

6. Hic-5 appears to enhance complex formation between MT1-MMP and FAK in activated endothelial cells, which likely coordinates matrix proteolysis and cell motility.

7. Hic-5 plays a central role in the positive feedback ROS-JNK signaling cascade that regulates hepatocellular carcinoma progression.

8. Hic-5 influences the genomic occupancy of multiple steroid receptors and thereby blocks some aspects of hormonal regulation.

9. Endothelial Hic-5 plays an important role in the formation of microvilli-like structures and in the interaction between ECs and monocytes, leading to monocyte recruitment and subsequent development of atherosclerosis.

10. Studies in vitro and in vivo using TGF-beta1 and TGFB1I1 shRNA demonstrated that TGFB1I1 is required for TGF-beta stimulated EMT that contributes to malignant progression of astrocytomas.

11. Hic-5 siRNA also suppressed TGF-beta2-induced fibrogenic activity and dexamethasone-induced myocilin expression in HTM cells.

12. Hic5 coordinates AR signaling with adhesion and extracellular matrix contacts to regulate cell behavior in the tumor microenvironment.

13. Hic-5 suppresses senescence and profibrotic activities of myofibroblasts by down-regulating Nox4 expression.

14. The ubiquitin ligase activity of Cbl-c by the direct interaction of the LIM zinc coordinating domain of Hic5 is demonstrated.

15. Hic-5 can potentially exercise multiple functions in growth, differentiation, migration and adhesion of keratinocytes, partially via nuclear-cell membrane shuttling.

16. the HIC-5- and KLF4-dependent mechanism transactivates p21(Cip1) in response to anchorage loss

17. It plays a roll in extracellular matrix remodeling and the signal transduction via reactive oxygen species. (review)

18. Findings suggest that hydrogen peroxide-inducible clone-5 (Hic-5) is involved in changes in the mesangial cells (MCs) phenotype to produce abnormal extracellular matrix remodeling in glomerulonephritis (GN).

19. these results provide the first evidence for a physical and mutual functional interaction between Hic-5 and the BMP signaling pathway.

20. Androgen receptor transactivity is potentiated by TGF-beta1 through Smad3 but checked by its coactivator Hic-5/ARA55 in balding dermal papilla cells.

Mouse (Murine) Transforming Growth Factor beta 1 Induced Transcript 1 (TGFB1I1) interaction partners

1. Together, the authors show the antagonistic regulation of the alpha-enhancer activity by Pax6 and the LIM protein complex is necessary for the establishment of an inner retinal circuitry, which controls visual adaptation.

2. Isolated Hic-5(-/-);PyMT CAFs were defective in stress fiber organization and exhibited reduced contractility. These cells also failed to efficiently deposit and organize the ECM in two and three dimensions. This, in turn, impacted three-dimensional MDA-MB-231 tumor cell migration behavior

3. paxillin and Hic-5 have both redundant and distinctive functions in invadosome formation.

4. Hic-5 deficiency attenuates the activation of hepatic stellate cells and liver fibrosis though reducing the TGF-beta/Smad2 signaling by upregulation of Smad7

5. Hic-5 regulates mesangial cell proliferation in proliferative glomerulonephritis in mice.

6. Endothelial Hic-5 plays an important role in the formation of microvilli-like structures and in the interaction between ECs and monocytes, leading to monocyte recruitment and subsequent development of atherosclerosis.

7. Hic-5 is a transcription coregulator that acts before and/or after glucocorticoid receptor genome occupancy in a gene-selective manner.

8. Hic-5 is expressed in B16-F1 murine melanoma cells.

9. identified Hic-5 as a novel and specific regulatory factor for thrombin-induced alphaIIbbeta3 activation and subsequent platelet aggregation in mice.

10. the HIC-5- and KLF4-dependent mechanism transactivates p21(Cip1) in response to anchorage loss

11. These data identify discrete roles for paxillin and Hic-5 in Rac1 and RhoA-dependent cell adhesion formation and maturation; processes essential for productive cell migration.

12. Transforming growth factor-beta1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein.

13. DNA-binding domain acetylation in the TR4 nuclear receptor by the coregulator ARA55 leads to suppression of TR4 transactivation

14. Findings indicate that Hic-5 may serve as a key regulator in mechanosensitive vascular remodeling.

15. Hic-5/ARA55 expression in response to castration-enabled epithelial regression through the repression of c-myc gene at the chromatin level.

16. These data suggest that the reduced expression of Hic-5 and concomitant reduced CTGF promoter activity may contribute to the anti-angiogenic effects of histone deacetylase inhibitors.

17. role in regulation of cellular phenotypes -review

18. Results suggest that paxillin and Hic-5 associate with GIT1 with different binding modes.

19. Results show that Hic-5 accumulates in the nucleus in response to oxidants such as hydrogen peroxide.

20. Important component in determining an epithelial differentiation program induced by PPARgamma.