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

1. Here we show genome-wide that blocked GBR generally require CHD9 and BRM (show SMARCA2 Proteins) 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.

2. Isolated Hic-5(-/-);PyMT CAFs (show TBX1 Proteins) were defective in stress fiber organization and exhibited reduced contractility. These cells also failed to efficiently deposit and organize the ECM (show MMRN1 Proteins) in two and three dimensions. This, in turn, impacted three-dimensional MDA-MB-231 tumor cell migration behavior

3. 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.

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

5. Hic-5 appears to enhance complex formation between MT1-MMP (show MMP14 Proteins) and FAK (show PTK2 Proteins) in activated endothelial cells, which likely coordinates matrix proteolysis and cell motility.

6. Hic-5 plays a central role in the positive feedback ROS (show ROS1 Proteins)-JNK (show MAPK8 Proteins) signaling cascade that regulates hepatocellular carcinoma progression.

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

8. 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.

9. Studies in vitro and in vivo using TGF-beta1 (show TGFB1 Proteins) and TGFB1I1 shRNA demonstrated that TGFB1I1 is required for TGF-beta (show TGFB1 Proteins) stimulated EMT (show ITK Proteins) that contributes to malignant progression of astrocytomas.

10. Hic-5 siRNA also suppressed TGF-beta2 (show TGFB2 Proteins)-induced fibrogenic activity and dexamethasone-induced myocilin (show MYOC Proteins) expression in HTM 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 (show PAX6 Proteins) and the LIM protein (show PDLIM1 Proteins) complex is necessary for the establishment of an inner retinal circuitry, which controls visual adaptation.

2. Isolated Hic-5(-/-);PyMT CAFs (show TBX1 Proteins) were defective in stress fiber organization and exhibited reduced contractility. These cells also failed to efficiently deposit and organize the ECM (show MMRN1 Proteins) in two and three dimensions. This, in turn, impacted three-dimensional MDA-MB-231 tumor cell migration behavior

3. paxillin (show PXN Proteins) 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 (show TGFB1 Proteins)/Smad2 (show SMAD2 Proteins) signaling by upregulation of Smad7 (show SMAD7 Proteins)

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 (show NR3C1 Proteins) 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 (show F2 Proteins)-induced alphaIIbbeta3 activation and subsequent platelet aggregation in mice.

10. the HIC-5- and KLF4 (show KLF4 Proteins)-dependent mechanism transactivates p21(Cip1 (show CDKN1A Proteins)) in response to anchorage loss