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Balancing cell numbers during organogenesis: Six1a differentially affects neurons and sensory hair cells in the inner ear
Six1a plays an essential role at the onset of fast muscle differentiation.
six1a and pax3 (show PAX3 Proteins) do not function in the same regulatory network. We proposed four putative regulatory pathways to understand how six1a distinctly interacts with either myf5 (show MYF5 Proteins) or myod (show MYOD1 Proteins) during zebrafish craniofacial muscle development.
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.
GATA1 (show GATA1 Proteins) may be a potential regulator of Six2-maintained population of nephron progenitor cells.
Six2 mediates the protective effects of GDNF on damaged DA neurons by regulating Smurf1 (show SMURF1 Proteins) expression.
Differentiation of nephron progenitors requires downregulation of Six2, a transcription factor required for progenitor maintenance, and that Notch (show NOTCH1 Proteins) signaling is necessary and sufficient for Six2 downregulation.
Zeb1 promotes proliferation and apoptosis and inhibits the migration of metanephric mesenchyme cells, in association with Six2.
In Six2-positive nephrogenic progenitors, GLI3 (show GLI3 Proteins) repressor decreased progenitor cell proliferation reducing the number of nephrogenic precursor structures in the Pallister-Hall syndrome mouse model.
Mechanistically, LIF (show LIF Proteins) activates STAT (show STAT1 Proteins), which binds to a Stat (show STAT1 Proteins) consensus sequence in the Six2 proximal promoter and sustains SIX2 levels.
Dicer (show DICER1 Proteins) ablation in the early metanephric mesenchyme results in severe renal dysgenesis despite normal initial specification of nephron progenitors and ureteric bud outgrowth.
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.
results reveal a functional link between Eya1 (show EYA1 Proteins), Six2, and Myc (show MYC Proteins) in driving the expansion and maintenance of the multipotent progenitors during nephrogenesis
Data show that three of the eight conserved noncoding sequences (CNSs) located within a 317-kb segment of the Six2 genomic locus were nephric enhancers.
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.
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.
elevated expressions of SIX2, SIX4 (show SIX4 Proteins), and SIX6 (show SIX6 Proteins) predicted poor overall survival (OS) in NSCLC and poor relapse-free survival (RFS) in lung adenocarcinoma
these findings delineate the important function of the TGFbeta (show TGFB1 Proteins) signaling pathway in the early development of kidney and TbetaRII was shown to be able to promote the expression of Six2 through Smad3 (show SMAD3 Proteins) mediating transcriptional regulation and in turn activate the proliferation of MM cells.
We suggest SIX2 haploinsufficiency as a potential congenital factor could be attributed to developmental malformation of the middle ear ossicles and upper eyelid.
SIX2 deletion is associated with frontonasal dysplasia syndrome.
SIX2 overexpression and concomitantly decreased promoter methylation.
in tumors with DGCR8 (show DGCR8 Proteins) E518K and DROSHA (show DROSHA Proteins) exon 29 (miRNAPG-HS) mutations ... greater prevalence of tumors with blastemal predominant histology in patients with miRNAPG-HS and/or SIX1 (show SIX1 Proteins)/2 Q177R mutations
Recurrent mutations included a hotspot mutation (Q177R) in the homeo-domain of SIX1 (show SIX1 Proteins) and SIX2 in tumors with high proliferative potential (18.1% of blastemal cases); mutations in the DROSHA (show DROSHA Proteins)/DGCR8 (show DGCR8 Proteins) microprocessor genes
Nuclear protein (show RDBP Proteins) & 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.
This gene is a member of the vertebrate gene family which encode proteins homologous to the Drosophila 'sine oculis' homeobox protein. The encoded protein is a transcription factor which, like other members of this gene family, may be involved in limb or eye development.
homeobox protein six1a
, homeobox protein six1b
, homeodomain transcription factor Six1b
, sine oculis homeobox homolog 1b
, sine oculis homeobox homolog 2
, homeobox protein SIX2
, sine oculis-related homeobox 2 homolog
, sine oculis-related homeobox 2