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ARHGAP22 Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q7Z5H3 |
| Other Accession | NP_067049.2 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 76779 Da |
| Antigen Region | 604-633 aa |
| Gene ID | 58504 |
|---|---|
| Other Names | Rho GTPase-activating protein 22, Rho-type GTPase-activating protein 22, ARHGAP22, RHOGAP2 |
| Target/Specificity | This ARHGAP22 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 604-633 amino acids from the C-terminal region of human ARHGAP22. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| 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 | ARHGAP22 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ARHGAP22 |
|---|---|
| Synonyms | RHOGAP2 |
| Function | Rho GTPase-activating protein involved in the signal transduction pathway that regulates endothelial cell capillary tube formation during angiogenesis. Acts as a GTPase activator for the RAC1 by converting it to an inactive GDP-bound state. Inhibits RAC1- dependent lamellipodia formation. May also play a role in transcription regulation via its interaction with VEZF1, by regulating activity of the endothelin-1 (EDN1) promoter (By similarity). |
| Cellular Location | Cytoplasm. Nucleus. Note=Mainly cytoplasmic. Some fraction is nuclear (By similarity) |
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Provided below are standard protocols that you may find useful for product applications.
Background
ARHGAPs, such as ARHGAP22, encode negative regulators of Rho GTPases (see ARHA; MIM 165390), which are implicated in actin remodeling, cell polarity, and cell migration (Katoh and Katoh, 2004 [PubMed 15254788]).
References
Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :
Dick, D.M., et al. Mol. Psychiatry (2010) In press :
Grupe, A., et al. Am. J. Hum. Genet. 78(1):78-88(2006)
Katoh, M., et al. Int. J. Mol. Med. 14(2):333-338(2004)
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