SLUG Antibody (N-term K9)
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS: 5
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | O43623 |
Other Accession | O08954, P97469, Q3MHQ4 |
Reactivity | Human |
Predicted | Bovine, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 29986 Da |
Antigen Region | 1-30 aa |
Gene ID | 6591 |
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Other Names | Zinc finger protein SNAI2, Neural crest transcription factor Slug, Protein snail homolog 2, SNAI2, SLUG, SLUGH |
Target/Specificity | This SLUG antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human SLUG. |
Dilution | WB~~1:1000 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | SLUG Antibody (N-term K9) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | SNAI2 |
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Synonyms | SLUG, SLUGH |
Function | Transcriptional repressor that modulates both activator- dependent and basal transcription. Involved in the generation and migration of neural crest cells. Plays a role in mediating RAF1-induced transcriptional repression of the TJ protein, occludin (OCLN) and subsequent oncogenic transformation of epithelial cells (By similarity). Represses BRCA2 expression by binding to its E2-box- containing silencer and recruiting CTBP1 and HDAC1 in breast cells. In epidermal keratinocytes, binds to the E-box in ITGA3 promoter and represses its transcription. Involved in the regulation of ITGB1 and ITGB4 expression and cell adhesion and proliferation in epidermal keratinocytes. Binds to E-box2 domain of BSG and activates its expression during TGFB1-induced epithelial-mesenchymal transition (EMT) in hepatocytes. Represses E-Cadherin/CDH1 transcription via E-box elements. Involved in osteoblast maturation. Binds to RUNX2 and SOC9 promoters and may act as a positive and negative transcription regulator, respectively, in osteoblasts. Binds to CXCL12 promoter via E-box regions in mesenchymal stem cells and osteoblasts. Plays an essential role in TWIST1-induced EMT and its ability to promote invasion and metastasis. |
Cellular Location | Nucleus. Cytoplasm. Note=Observed in discrete foci in interphase nuclei. These nuclear foci do not overlap with the nucleoli, the SP100 and the HP1 heterochromatin or the coiled body, suggesting SNAI2 is associated with active transcription or active splicing regions |
Tissue Location | Expressed in most adult human tissues, including spleen, thymus, prostate, testis, ovary, small intestine, colon, heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas. Not detected in peripheral blood leukocyte. Expressed in the dermis and in all layers of the epidermis, with high levels of expression in the basal layers (at protein level). Expressed in osteoblasts (at protein level). Expressed in mesenchymal stem cells (at protein level) Expressed in breast tumor cells (at protein level) |
Provided below are standard protocols that you may find useful for product applications.
Background
SLUG is a member of the Snail family of C2H2-type zinc finger transcription factors. This protein acts as a transcriptional repressor that binds to E-box motifs and is also likely to repress E-cadherin transcription in breast carcinoma. This protein is involved in epithelial-mesenchymal transitions and has antiapoptotic activity. Mutations in the gene encoding SLUG may be associated with sporadic cases of neural tube defects.
References
Sanchez-Martin, M., et al., Hum. Mol. Genet. 11(25):3231-3236 (2002).
Hajra, K.M., et al., Cancer Res. 62(6):1613-1618 (2002).
Hemavathy, K., et al., Mol. Cell. Biol. 20(14):5087-5095 (2000).
Inukai, T., et al., Mol. Cell 4(3):343-352 (1999).
Cohen, M.E., et al., Genomics 51(3):468-471 (1998).
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