癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
SALL1 Rabbit pAb
- 产品详情
- 实验流程
Application 
| IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | Q9NSC2 |
| Other Accession | Q9NSC2 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 140405 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human SALL1 |
| Epitope Specificity | 451-550/1324 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SIMILARITY | Belongs to the sal C2H2-type zinc-finger protein family. Contains 9 C2H2-type zinc fingers. |
| SUBUNIT | Interacts with HDAC1, HDAC2, RBBP4, RBPP7, MTA1 and MTA2. Interacts with FAM58A. Probably associates with NuRD histone deacetylase complex (HDAC). |
| 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 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. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | 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. |
| Gene ID | 6299 |
|---|---|
| Other Names | SAL1; Spalt; HEL-S-89; HSAL1; Sal-1; TBS; ZNF794; Msal-3; SALL1_HUMAN; SALL1; Spalt-like transcription factor 1; Zinc finger protein 794; Zinc finger protein SALL1; Zinc finger protein Spalt-1 (HSal1 | Sal-1); SALL1_MOUSE; Zinc finger protein Spalt-3 (Sal-3 | mSal-3); Sal3; spalt like transcription factor 1; sal (Drosophila)-like 1; sal-like 1 (Drosophila) |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | SALL1 |
|---|---|
| Synonyms | SAL1, ZNF794 |
| Function | Transcriptional repressor involved in organogenesis. Plays an essential role in ureteric bud invasion during kidney development. |
| Cellular Location | Nucleus {ECO:0000250|UniProtKB:Q9ER74}. |
| Tissue Location | Highest levels in kidney. Lower levels in adult brain (enriched in corpus callosum, lower expression in substantia nigra) and liver |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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