Browse our HOP Homeobox Proteins (HOPX)

Human HOP Homeobox (HOPX) interaction partners

1. In the present study, we compared the 2 potential epigenetic prognostic markers of CDO1 hypermethylation and HOPX hypermethylation using the same breast cancer samples, and the final focus was given on CDO1 hypermethylation

2. Data suggest that HOP homeobox HOPX (HOPX) acts as a tumour suppressor via the epigenetic regulation of snail family transcription factors (SNAIL) transcription and a prognostic biomarker for nasopharyngeal carcinoma (NPC) metastasis and therapeutic target for NPC treatment.

3. HOPX functions as a tumour suppressor in HNSCC and suggest a central role for HOPX in suppressing epithelial carcinogenesis

4. The association between the MEEVD C-terminal peptide from the heat shock protein 90 (Hsp90) and tetratricopeptide repeat A (TPR2A) domain of the heat shock organizing protein (Hop) is a useful prototype to study the fundamental molecular details about the Hop-Hsp90 interaction. Observed are conformational changes of the peptide and the protein receptor induced by binding. The binding free energy is 8.4 kcal/mol.

5. HOPX is functionally regulated by SCL in hematoendothelial differentiation of mesoderm progenitor cells.

6. HOPX is a distinctive homeobox gene with characteristic clinical and biological implications and its expression is a powerful predictor of prognosis in AML patients.

7. HOPX has a role in the pathogenesis of skin cancers and skin diseases.

8. these data indicate that the disruption of the PrP(C)-HOP complex could be a potential therapeutic target for modulating the migratory and invasive cellular properties that lead to metastatic Colorectal cancer (CRC).

9. HOPX promoter methylation is not only frequent and cancer-specific but also associated with aggressive phenotype in breast cancer.

10. Computational results identified HOPX gene as a new potential driver for ovarian carcinogenesis.

11. The results suggest that HOPX may contribute to pathogenesis or manifestation of hypertrophic cardiomyopathy as a modifier gene.

12. Data show that binding of heat shock proteins Hsp70 and Hsp90 requires prior binding of Hop protein to Hsp90.

13. HOPX is methylated and exerts tumour-suppressive function through Ras-induced senescence in human lung cancer.

14. GATA6 and HOPX are critical nodes in a lineage-selective pathway that directly links effectors of airway epithelial specification to the inhibition of metastasis in the lung ADC subtype.

15. HOPX-beta promoter methylation is a frequent and cancer-specific event in CRC progression.

16. Knockdown of Hop caused a decrease in the level of RhoC GTPase, and significantly inhibited pseudopodia formation in Hs578T cells. Our data suggest that Hop regulates directional cell migration by multiple unknown mechanisms.

17. HOPX/Hopx expression is reduced in multiple examples of human and murine cardiac hypertrophy and failure.

18. results identify distinct functions for the Hop cochaperone, revealing an asymmetric mechanism for Hsp90 regulation and client loading

19. HOP is a novel modulator of late terminal differentiation in keratinocytes

20. Hopx regulates the expression of genes involved in regulation of apoptosis and survival and makes them refractory to Fas-induced apoptosis.

Mouse (Murine) HOP Homeobox (HOPX) interaction partners

1. Hopx is required and sufficient, respectively, for basal radial glial cells abundance as found in the developing gyrencephalic neocortex.

2. Analysis of the hematopoietic stem/progenitor cell pool in Hopx-/- mice demonstrated significantly reduced cell frequencies and impaired engraftment in competitive repopulation assays, thus providing functional validation of this positional candidate gene

3. Type I alveolar cells expressing Hopx manifest plasticity to regenerate type II alveolar cells in the lung.

4. Peripherally Induced Tolerance Depends on Peripheral Regulatory T Cells That Require Hopx To Inhibit Intrinsic IL-2 Expression.

5. Hopx integrates Bmp and Wnt signaling by physically interacting with activated Smads and repressing Wnt genes.

6. Hopx expression defines a subset of multipotent hair follicle stem cells and a progenitor population primed to give rise to K6+ niche cells.

7. HOPX/Hopx expression is reduced in multiple examples of human and murine cardiac hypertrophy and failure.

8. Hopx regulates the expression of genes involved in regulation of apoptosis and survival and makes them refractory to Fas-induced apoptosis.

9. Hopx is required for the function of regulatory T cells induced by DCs and the promotion of DC-mediated T cell unresponsiveness in vivo.

10. Hdac2, Hopx, and Gata4 coordinately regulate cardiac myocyte proliferation during embryonic development.

11. Expressed in embryonic myocardium and other mesoderm, but not in endocardium or great vessels.

12. data show that Hop can inhibit serum response factor-dependent transcriptional activation by recruiting histone deacetylase (HDAC) activity and can form a complex that includes HDAC2

13. Hop functions in the adult cardiac conduction system and demonstrate conservation of molecular hierarchies between embryonic myocardium and the specialized conduction tissue of the mature heart.

14. Hop is regulated in the forebrain by a so far unidentified paracrine signaling factor from the roof plate

15. Expression pattern of Hop provides first evidence that new transcription is initiated in lens fiber cells after they detach from the capsule. Hop may be first of class of genes with this pattern of expression.

16. HOP/NECC1 (-/-) placenta exhibited marked propagation of giant cell layers and, in turn reduction of spongiotrophoblast formation

17. HOP participates in the regulation of the adult mouse hippocampal stem cell niche by negatively affecting cell survival

18. HOP is highly expressed in the developing heart, dependent on the cardiac-restricted homeodomain protein Nkx2.5. Mice homozygous for a HOP null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes.

19. Inactivation of Hop in mice by homologous recombination results in a partially penetrant embryonic lethal phenotype with severe developmental cardiac defects involving the myocardium.