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>   home   >   Products   >   Primary Antibodies   >   Signal Transduction   >   GPR161 Antibody (Cytoplasmic Domain)   

GPR161 Antibody (Cytoplasmic Domain)

Rabbit Polyclonal Antibody

     
  • IHC - GPR161 Antibody (Cytoplasmic Domain) ALS10090
    Anti-GPR161 antibody IHC of human spleen.
  • IHC - GPR161 Antibody (Cytoplasmic Domain) ALS10090
    Anti-GPR161 antibody IHC of human adrenal.
  • SPECIFICATION
  • CITATIONS
  • PROTOCOLS
  • BACKGROUND
Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
IHC-P
Primary Accession Q8N6U8
Reactivity Human, Hamster, Monkey
Host Rabbit
Clonality Polyclonal
Calculated MW 59kDa
Dilution IHC-P (2-3 µg/ml)
Additional Information
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, except MAGEA10 (63%).
Reconstitution & Storage Long term: -70°C; Short term: +4°C
PrecautionsGPR161 Antibody (Cytoplasmic Domain) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
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
Research Areas
Citations (0)

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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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$ 395.00
Cat# ALS10090
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