SIX Homeobox 2 Proteine (SIX2)

Human SIX Homeobox 2 (SIX2) Interaktionspartner

1. Six2 is negatively correlated with good prognosis and decreases 5-FU sensitivity via suppressing E-cadherin expression in HCC cells.

2. the phenotypic spectrum of SIX2 haploinsufficiency is widened. Moreover, 2p21 microdeletions with SIX2 haploinsufficiency appear to lead to a recognizable phenotype with facial features resembling blepharophimosis-ptosis-epicanthus inversus syndrome.

3. DDX3-mediated colorectal cancer aggressiveness and cetuximab resistance were regulated by the YAP1/SIX2 axis in KRAS-wild type cells and further confirmed in animal models.

4. elevated expressions of SIX2, SIX4, and SIX6 predicted poor overall survival (OS) in NSCLC and poor relapse-free survival (RFS) in lung adenocarcinoma

5. these findings delineate the important function of the TGFbeta signaling pathway in the early development of kidney and TbetaRII was shown to be able to promote the expression of Six2 through Smad3 mediating transcriptional regulation and in turn activate the proliferation of MM cells.

6. We suggest SIX2 haploinsufficiency as a potential congenital factor could be attributed to developmental malformation of the middle ear ossicles and upper eyelid.

7. SIX2 deletion is associated with frontonasal dysplasia syndrome.

8. These data suggest differential SIX-factor regulation might have contributed to species differences in nephron progenitor programs such as the duration of nephrogenesis and the final nephron count

9. SIX2 overexpression and concomitantly decreased promoter methylation.

10. in tumors with DGCR8 E518K and DROSHA exon 29 (miRNAPG-HS) mutations ... greater prevalence of tumors with blastemal predominant histology in patients with miRNAPG-HS and/or SIX1/2 Q177R mutations

11. Recurrent mutations included a hotspot mutation (Q177R) in the homeo-domain of SIX1 and SIX2 in tumors with high proliferative potential (18.1% of blastemal cases); mutations in the DROSHA/DGCR8 microprocessor genes

12. Nuclear protein & mRNA expression of SIX2 were similar across all stages of disease, in favorable or unfavorable histology & in treatment failure or success. It is not found in normal kidney.

13. Lack of mutations in the coding regions of SIX2 among the sporadic microtia patients

14. Defects in these proteins could affect kidney development at multiple stages, leading to the congenital anomalies observed in patients with renal hypodysplasia