SIX Homeobox 2 Proteine (SIX2)

Human SIX Homeobox 2 (SIX2) Interaktionspartner

1. 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.

2. 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.

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

4. these findings delineate the important function of the TGFbeta (zeige TGFB1 Proteine) signaling pathway in the early development of kidney and TbetaRII was shown to be able to promote the expression of Six2 through Smad3 (zeige SMAD3 Proteine) mediating transcriptional regulation and in turn activate the proliferation of MM cells.

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

6. SIX2 deletion is associated with frontonasal dysplasia syndrome.

7. SIX2 overexpression and concomitantly decreased promoter methylation.

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

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

10. Nuclear protein (zeige RDBP Proteine) & 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.

Mouse (Murine) SIX Homeobox 2 (SIX2) Interaktionspartner

1. 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.

2. GATA1 (zeige GATA1 Proteine) may be a potential regulator of Six2-maintained population of nephron progenitor cells.

3. Six2 mediates the protective effects of GDNF on damaged DA neurons by regulating Smurf1 (zeige SMURF1 Proteine) expression.

4. Differentiation of nephron progenitors requires downregulation of Six2, a transcription factor required for progenitor maintenance, and that Notch (zeige NOTCH1 Proteine) signaling is necessary and sufficient for Six2 downregulation.

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

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

7. Mechanistically, LIF (zeige LIF Proteine) activates STAT (zeige STAT1 Proteine), which binds to a Stat (zeige STAT1 Proteine) consensus sequence in the Six2 proximal promoter and sustains SIX2 levels.

8. Dicer (zeige DICER1 Proteine) ablation in the early metanephric mesenchyme results in severe renal dysgenesis despite normal initial specification of nephron progenitors and ureteric bud outgrowth.

9. 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.

10. results reveal a functional link between Eya1 (zeige EYA1 Proteine), Six2, and Myc (zeige MYC Proteine) in driving the expansion and maintenance of the multipotent progenitors during nephrogenesis