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

Mouse (Murine) SIX Homeobox 2 (SIX2) Interaktionspartner

1. Reveal a unique dose response of nephron progenitors to the level of SIX2 protein in which the role of SIX2 in progenitor proliferation versus self-renewal is separable.

2. Embryonic day 18.5 Six2Frs2alphaKO kidneys were hypoplastic and not cystic, postnatal day (P) 7 mutants had proximal tubular-derived cysts that nearly replaced the renal parenchyma by P21. Mutants had high proximal tubular proliferation rates and interstitial fibrosis, similar to known polycystic kidney disease models.

3. GATA1 may be a potential regulator of Six2-maintained population of nephron progenitor cells.

4. Six2 mediates the protective effects of GDNF on damaged DA neurons by regulating Smurf1 expression.

5. Differentiation of nephron progenitors requires downregulation of Six2, a transcription factor required for progenitor maintenance, and that Notch signaling is necessary and sufficient for Six2 downregulation.

6. Zeb1 promotes proliferation and apoptosis and inhibits the migration of metanephric mesenchyme cells, in association with Six2.

7. In Six2-positive nephrogenic progenitors, GLI3 repressor decreased progenitor cell proliferation reducing the number of nephrogenic precursor structures in the Pallister-Hall syndrome mouse model.

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. Mechanistically, LIF activates STAT, which binds to a Stat consensus sequence in the Six2 proximal promoter and sustains SIX2 levels.

10. Dicer ablation in the early metanephric mesenchyme results in severe renal dysgenesis despite normal initial specification of nephron progenitors and ureteric bud outgrowth.

11. miR181c downregulates the expression of Six2, restrain the proliferation and promote the apoptosis that even makes the nephron progenitor phenotype lose MM cells, suggesting a potential role of miR181c during the kidney development.

12. results reveal a functional link between Eya1, Six2, and Myc in driving the expansion and maintenance of the multipotent progenitors during nephrogenesis

13. Our findings establish Six2 as a regulator of metastasis in human breast cancers and demonstrate an epigenetic function for SIX family transcription factors in metastatic progression through the regulation of E-cadherin.

14. These results implied that inhibition of Nf1 may delay metanephros development via down-regulation of Six2.

15. Osr1 plays crucial roles in Six2-dependent maintenance of nephron progenitors during mammalian nephrogenesis.

16. this study concluded that by targeting the transcription factor gene Six2, miR-181b inhibits the proliferation of metanephric mesenchymal cells in vitro and might play an important role in the formation of nephrons.

17. Six1 and Six2 are complementarily but asymmetrically expressed in the peri-cloacal mesenchymal progenitors and are critical for correct genitor-urinary and digestive organs body patterning.

18. Wnt and BMP signaling cooperate with Hox in the control of Six2 expression in limb tendon precursor.

19. The Six2 and Lef/Tcf factors form a regulatory complex that promotes progenitor maintenance while entry of beta-catenin into this complex promotes nephrogenesis.

20. Results demonstrate impaired osmoregulatory mechanisms consistent with chronic renal failure in the Br/+ mouse and indicate that six2 haploinsufficiency has a direct effect on postnatal fluid and electrolyte handling associated with fluid imbalance.