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VPS39 Antibody (C-Terminus)
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF |
|---|---|
| Primary Accession | Q96JC1 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 102kDa |
| Dilution | IHC-P (5 µg/ml), WB (0.5-1 µg/ml), |
| Gene ID | 23339 |
|---|---|
| Other Names | Vam6/Vps39-like protein, TRAP1-like protein, hVam6p, VPS39, KIAA0770, TLP, VAM6 |
| Target/Specificity | Human VPS39. At least four isoforms of VPS39 are known to exist; this antibody will detect all four. VPS39 antibody is predicted not to cross-react with TRAP1. |
| Reconstitution & Storage | Short term 4°C, long term aliquot and store at -20°C, avoid freeze thaw cycles. Store undiluted. |
| Precautions | VPS39 Antibody (C-Terminus) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | VPS39 (HGNC:20593) |
|---|---|
| Synonyms | KIAA0770, TLP, VAM6 |
| Function | Regulator of TGF-beta/activin signaling, inhibiting SMAD3- and activating SMAD2-dependent transcription. Acts by interfering with SMAD3/SMAD4 complex formation, this would lead to inhibition of SMAD3-dependent transcription and relieve SMAD3 inhibition of SMAD2-dependent promoters, thus increasing SMAD2- dependent transcription. Does not affect TGF-beta-induced SMAD2 or SMAD3 phosphorylation, nor SMAD2/SMAD4 complex formation. |
| Cellular Location | Cytoplasm. Lysosome membrane; Peripheral membrane protein. Late endosome membrane; Peripheral membrane protein. Note=Colocalizes with TGFBR1 and TGFBR2 in cytoplasmic vesicular structures and most prominently in cortical vesicles. |
| Tissue Location | Widely expressed, with highest levels in heart, skeletal muscle, kidney, pancreas, brain, placenta and spleen |
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Provided below are standard protocols that you may find useful for product applications.
Background
May play a role in clustering and fusion of late endosomes and lysosomes. Regulator of TGF-beta/activin signaling, inhibiting SMAD3- and activating SMAD2-dependent transcription. Acts by interfering with SMAD3/SMAD4 complex formation, this would lead to inhibition of SMAD3-dependent transcription and relieve SMAD3 inhibition of SMAD2-dependent promoters, thus increasing SMAD2-dependent transcription. Does not affect TGF-beta-induced SMAD2 or SMAD3 phosphorylation, nor SMAD2/SMAD4 complex formation.
References
Caplan S.,et al.J. Cell Biol. 154:109-122(2001).
Dell'Angelica E.C.,et al.Submitted (JUN-2000) to the EMBL/GenBank/DDBJ databases.
Nagase T.,et al.DNA Res. 5:277-286(1998).
Nakajima D.,et al.DNA Res. 9:99-106(2002).
Bechtel S.,et al.BMC Genomics 8:399-399(2007).
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