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Data show that both sall1 and sall4 (Montrer SALL4 Kits ELISA) act to repress pou5f3 (oct4)family gene expression in the neural plate, thereby allowing vertebrate neural development to proceed.
Inhibition of SALL1 correlates with reduced levels of CDH1 (Montrer CDH1 Kits ELISA), an important contributor to epithelial-to-mesenchymal transition.
quantity and quality of SALL1 transcript are important for SALL1 function and determine phenotype, and mode of inheritance, of allelic SALL1-related disorders
report on a family with features of TBS in whom a novel 149 kb deletion spanning the SALL1 gene was identified by high resolution cytogenetics SNP microarray
novel role for Sall1 as a member of the transcriptional network that regulates stem cell pluripotency
Sall1 induces angiogenesis by stimulating VEGF-A (Montrer VEGFA Kits ELISA) promoter activity.
Studies indicate that vertebrate sal orthologues (spalt-like/sall) have important developmental roles during neural development and organogenesis and gentic diseases.
Mutation in Townes-Brocks syndrome. Product is a transcriptional repressor which interacts with TRF1/PIN2 (Montrer TERF1 Kits ELISA) and localizes to pericentromeric heterochromatin.
binding of proteins SALL1, UBE2I (Montrer UBE2I Kits ELISA) and SUMO-1 (Montrer SUMO1 Kits ELISA)
sall1 enhances the canonical Wnt (Montrer WNT2 Kits ELISA) signaling by localizing to heterochromatin
analysis of SALL1 mutations in Townes-Brocks syndrome
These findings highlight an important function of Sall1-NuRD interaction in the regulation of Six2 (Montrer SIX2 Kits ELISA)-positive multipotent renal progenitor cells and formation of the loop of Henle.
this study shows that transcriptional regulation by Sall1 maintains microglial identity and physiological properties in the central nervous system and allows microglia-specific manipulation in vivo
Our study demonstrates that Sall1 marks Cardiac progenitor cells in an undifferentiated state and regulates cardiac differentiation
the expression of Sall1 in stromal progenitors restricts the excessive expansion of nephron progenitors in a non-cell autonomous manner, and Sall1-mediated regulation of Decorin and Fat4 might at least partially underlie the pathogenesis.
establish a functional role for Sall1 in the response of the adult kidney to acute injury
Dicer (Montrer DICER1 Kits ELISA) ablation in the early metanephric mesenchyme results in severe renal dysgenesis despite normal initial specification of nephron progenitors and ureteric bud outgrowth.
Sall1 activates progenitor-related genes in Six2 (Montrer SIX2 Kits ELISA)-positive nephron progenitors and represses gene expression in Six2 (Montrer SIX2 Kits ELISA)-negative differentiating nascent nephrons.
The findings highlight a novel role for Sall1 in maintaining the stemness of the progenitor cell pool by restraining their differentiation into renal vesicles.
These findings present novel insights into the function of Sall1 in the developing mouse cortex and provide avenues for future research into potential neural deficits in individuals with Townes-Brocks syndrome.
Sall1-expressing cells are present in the adult mouse kidney, predominantly in the proximal tubules. Sall1-expressing cells proliferate following Ischemia-reperfusion injury.
The protein encoded by this gene is a zinc finger transcriptional repressor and may be part of the NuRD histone deacetylase complex (HDAC). Defects in this gene are a cause of Townes-Brocks syndrome (TBS) as well as bronchio-oto-renal syndrome (BOR). Two transcript variants encoding different isoforms have been found for this gene.
, sal-like 1 b
, sal-like 1 (Drosophila)
, sal-like protein 1
, spalt-like transcription factor 1
, zinc finger protein 794
, zinc finger protein SALL1
, zinc finger protein Spalt-1
, zinc finger protein Spalt-3
, spalt 1
, transcription factor Spalt