Thermo Fisher Scientific SALL1 Polyclonal Antibody

Applications

Tested Dilution

Publications

Immunohistochemistry (Paraffin) (IHC (P))

1:50-1:200

-

Immunocytochemistry (ICC/IF)

0.25-2 µg/mL

-

Product Specifications

Species Reactivity

Human

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

Recombinant protein corresponding to Human SALL1. Recombinant protein control fragment (Product #RP-101166). if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:SALL1,uniProtId:Q9NSC2-1,ncbiNodeId:9606,antigenRange:562-636,antigenLength:1324,antigenImageFileName:PA5-62057_SALL1_Q9NSC2-1_Rabbit.svg,antigenImageFileNamePDP:PA5-62057_SALL1_Q9NSC2-1_Rabbit_PDP.jpeg,sortOrder:2}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

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Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

0.10 mg/mL

Purification

Antigen affinity chromatography

Storage buffer

PBS, pH 7.2, with 40% glycerol

Contains

0.02% sodium azide

Storage conditions

Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

Shipping conditions

Wet ice

RRID

AB_2646913

Product Specific Information

Immunogen sequence: TLPSLIPFIK TEEPAPIPIS HSATSPPGSV KSDSGGPESA TRNLGGLPEE AEGSTLPPSG GKSEESGMVT NSVPT

Highest antigen sequence identity to the following orthologs: Mouse - 75%, Rat - 75%.

Target Information

Sall1, which encodes a zinc finger protein, functions as a transcriptional repressor and interacts physically with histone deacetylase and other components of the chromatin remodeling NuRD complex. It is unknown whether the transcriptional repression is solely dependent on histone deacetylase activity. Gene expression profiling has identified Sall1 as a microglial signature gene. Microglia are the resident macrophages of the central nervous system (CNS). Sall1 is also expressed in abundance in the mesenchyme-derived structure from condensed mesenchyme, S-comma-shaped bodies, to renal tubules and podocytes. Sall1 has been identified as a key transcription factor in self-renewal renal progenitor cells. Sall1 is required to maintain the stemness of nephron progenitor cells by restraining their differentiation into renal vesicles. Defects in SALL1 are the cause of Townes-Brocks syndrome as well as bronchio-oto-renal syndrome. Heterozygous mutations of human SALL1 leading to Townes-Brocks syndrome features dysplastic ears, preaxial polydactyly, imperforate anus, and less commonly, kidney and heart anomalies (Kohlhase et al. 1998). Two transcript variants encoding different isoforms have been found for this gene.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.