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GPR161 Antibody (N-Terminus)
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, ICC |
|---|---|
| Primary Accession | Q8N6U8 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 59kDa |
| Dilution | IHC-P (4-9 µg/ml) |
| Gene ID | 23432 |
|---|---|
| Other Names | G-protein coupled receptor 161, G-protein coupled receptor RE2, GPR161 |
| Target/Specificity | Human GPR161. BLAST analysis of the peptide immunogen showed no homology with other human proteins. |
| Reconstitution & Storage | Long term: -70°C; Short term: +4°C |
| Precautions | GPR161 Antibody (N-Terminus) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | GPR161 |
|---|---|
| Function | Key negative regulator of Shh signaling, which promotes the processing of GLI3 into GLI3R during neural tube development. Recruited by TULP3 and the IFT-A complex to primary cilia and acts as a regulator of the PKA-dependent basal repression machinery in Shh signaling by increasing cAMP levels, leading to promote the PKA-dependent processing of GLI3 into GLI3R and repress the Shh signaling. In presence of SHH, it is removed from primary cilia and is internalized into recycling endosomes, preventing its activity and allowing activation of the Shh signaling. Its ligand is unknown (By similarity). |
| Cellular Location | Cell projection, cilium membrane; Multi-pass membrane protein. Cell membrane; Multi-pass membrane protein. Note=Mainly localizes to primary cilium in a TULP3 and IFT-A complex-dependent manner. In presence of SHH, it is removed from primary cilia and is internalized into recycling endosomes and is apparently not degraded (By similarity). |
| Volume | 50 µl |
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Provided below are standard protocols that you may find useful for product applications.
Background
Key negative regulator of Shh signaling, which promotes the processing of GLI3 into GLI3R during neural tube development. Recruited by TULP3 and the IFT-A complex to primary cilia and acts as a regulator of the PKA-dependent basal repression machinery in Shh signaling by increasing cAMP levels, leading to promote the PKA-dependent processing of GLI3 into GLI3R and repress the Shh signaling. In presence of SHH, it is removed from primary cilia and is internalized into recycling endosomes, preventing its activity and allowing activation of the Shh signaling. Its ligand is unknown (By similarity).
References
Warren C.N.,et al.Submitted (APR-2003) to the EMBL/GenBank/DDBJ databases.
Raming K.,et al.Recept. Channels 6:141-151(1998).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Gregory S.G.,et al.Nature 441:315-321(2006).
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