Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human SALL1 Antibodies:
anti-Mouse (Murine) SALL1 Antibodies:
anti-Rat (Rattus) SALL1 Antibodies:
Go to our pre-filtered search.
Dog (Canine) Polyclonal SALL1 Primary Antibody for ELISA - ABIN547919
Wang, Rao, Chu, Shen, Levasseur, Theunissen, Orkin: A protein interaction network for pluripotency of embryonic stem cells. in Nature 2006
Human Polyclonal SALL1 Primary Antibody for ELISA - ABIN4351912
Barry, Reddy: The association of an epibulbar dermoid and Duane syndrome in a patient with a SALL1 mutation (Townes-Brocks Syndrome). in Ophthalmic genetics 2008
SALL1 mutations might cause Townes-Brocks Syndrome.
Inhibition of SALL1 correlates with reduced levels of CDH1, 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 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 and localizes to pericentromeric heterochromatin.
binding of proteins SALL1, UBE2I and SUMO-1
sall1 enhances the canonical Wnt signaling by localizing to heterochromatin
analysis of SALL1 mutations in Townes-Brocks syndrome
Sall1 is essential for ureteric bud invasion, the initial key step for metanephros development
there is a different contribution of SALL1 gene function to mouse and human embryonic development
Data show that SALL1 contains two repression domains, one located at the extreme N-terminus of the protein and the other in the central region.
SALL1 is a likely target gene for SIX1 during kidney development
There is an enhancer element in the SALL1 gene.
SALL1 gene, mutations of which result in the Townes-Brocks phenotype, is expressed in the developing kidney.
SALL1 and GLI3 may have roles in limb malformation and are affected by nonsense-mediated decay
analysis of one sporadic case of Townes-Brocks syndrome for SALL1 gene mutations and review of the literature [review]
truncated SALL1 protein is expressed in cells derived from a TBS patient
demonstrate in vivo that the conditional overexpression of Ifng in metanephric mesenchymal (MM) progenitors results in renal agenesis or hypoplasia. Cell death was observed in and around the MM region of E10.5-11.5 mutants where Ifng was constitutively expressed during early kidney development and resulted in retardation of branching morphogenesis. Expression of Sall1 was decreased in the MM of mutant kidneys.
The data of this study indicated that Sall1 regulates microglial morphology during development.
Data suggest that Sall1 is associated with actin reorganization, endoplasmic reticulum stress, and apoptosis in podocytes injured by adriamycin, a topoisomerase II inhibitor used as antineoplastic antibiotic known to cause nephrosis and glomerulosclerosis.
These findings highlight an important function of Sall1-NuRD interaction in the regulation of Six2-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 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-positive nephron progenitors and represses gene expression in Six2-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.
studies indicate that Sall1-dependent signals from the metanephric mesenchyme are required to modulate ureteric bud tip Wnt patterning in order to initiate branching.
Data show that the Sall1CreER(T2) mouse is a valuable tool for in vivo time-dependent and region-specific knockout and overexpression studies.
overexpression of Sall1 does not affect kidney development, but does lead to a reduced body weight, suggesting that the optimal dosage of Sall1 is required for normal mouse development.
role in repression of transcription by recruiting a histone deacetylase complex
Truncated Sall1 transcriptional repressor is responsible for Townes-Brocks syndrome birth defects
Data show that both sall1 and sall4 act to repress pou5f3 (oct4)family gene expression in the neural plate, thereby allowing vertebrate neural development to proceed.
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 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
, sal-like 1
, sal-like 1 b
, sal-like 1 (Drosophila)