锌指转录蛋白Sall1抗体
规格：1mg/1ml
英文名： SALL1
别名： HSal1; Sal like protein 1; Sal-1; Sal-like protein 1; Sal1; SALL1; SALL1_HUMAN; Spalt like transcription factor 1; Spalt-like transcription factor 1; TBS; Townes Brocks syndrome; Zinc finger protein 7
分子量： 140kDa
储存液：0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glyce
克隆类型：Polyclonal
亚型：IgG
纯化方法：affinity purified by Protein A
**原：KLH conjugated synthetic peptide derived from human SALL1 (4
交叉反应：Human, Mouse, Rat, Chicken, Dog, Cow, Horse, Rabbit, Sheep,
细胞定位：细胞核
锌指转录蛋白Sall1抗体产品介绍：background: Sall1 and Sall2 are mammalian homologs of the Drosophila region-specific home-otic gene spalt (sal), which encodes a zinc finger-containing transcription regulator. Drosophila spalt (sal) is an essential genetic component required for the specification of posterior head and anterior tail as opposed to trunk. Mammalian Sall1 may mediate higher order chromatin structure, and may be a component of a distinct heterochromatin-dependent silencing process. Sall1 is present in kidney, brain and liver. Sall2 is a p53-independent regulator of p21 and BAX, and can function in some cell types as a regulator of cell growth and survival. Human Sall2 is present in brain, heart, kidney or pancreas. Sall1 and Sall2 are expressed in different areas of the fetal brain that may represent distinct sets of neurons. Function锌指转录蛋白Sall1抗体: Transcriptional repressor involved in organogenesis. Subunit: Interacts with HDAC1, HDAC2, RBBP4, RBPP7, MTA1 and MTA2. Interacts with FAM58A. Probably associates with NuRD histone deacetylase complex (HDAC). Subcellular Location: Nucleus. Tissue Specificity: Highest levels in kidney. Lower levels in ***** brain (enriched in corpus callosum, lower expression in substantia nigra) and liver. DISEASE: Defects in SALL1 are the cause of Townes-Brocks syndrome (TBS) [MIM:107480]. TBS is a rare, autosomal dominant malformation syndrome with a combination of imperforate anus, triphalangeal and supernumerary thumbs, malformed ears and sensorineural hearing loss. Defects in SALL1 may cause a锌指转录蛋白Sall1抗体phenotype overlapping with TBS, similar to bronchio-oto-renal syndrome (BOR) [MIM:113650]. BOR is an autosomal dominant disorder, manifested by various combinations of preauricular pits, branchial fistulae or cysts, lacrimal duct stenosis, hearing loss, structural defects of the outer, middle, or inner ear, and renal dysplasia. Associated defects include asthenic habitus, long narrow facies, constricted palate, deep overbite, and myopia. Hearing loss may be due to Mondini type cochlear defect and stapes fixation. Similarity: Belongs to the sal C2H2-type zinc-finger protein family. Contains 9 C2H2-type zinc fingers. Database links: UniProtKB/Swiss-Prot: Q9NSC2.2 Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
锌指转录蛋白Sall1抗体产品应用：WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500 （石蜡切片需做抗原修复） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
研究领域：细胞生物 发育生物学 转录调节因子 锌指蛋白 表观遗传学
储存条件： Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
来源： Rabbit
外观： Lyophilized or Liquid