Description:

Size: 100ul

Catalog no.: bs-15385R-A555

Price: 380 EUR

Product details

Modification Site

None

Gene ID Number

23432

Swiss Prot

Q8N6U8

Target Antigen

GPR161

French translation

anticorps

Tested applications

IF(IHC-P)

Clonality

Polyclonal

Modification

Unmodified

Excitation emission

553nm/568nm

Immunogen range

165-190/529

Concentration

1ug per 1ul

Subcellular location

Extracellular

Crossreactivity

Human, Mouse, Rat

Conjugated with

ALEXA FLUOR® 555

Clone

Polyclonal antibody

Recommended dilutions

IF(IHC-P)(1:50-200)

Purification

Purified by Protein A.

Conjugation

Alexa Fluor,ALEXA FLUOR 555

Category

Conjugated Primary Antibodies

Host Organism

Rabbit (Oryctolagus cuniculus)

Also known as

Anti-GPR161 PAb ALEXA FLUOR 555

Specificity

This is a highly specific antibody against GPR161.

Long name

GPR161 Polyclonal Antibody, ALEXA FLUOR 555 Conjugated

Synonyms

RE2; G-protein coupled receptor 161; G-protein coupled receptor RE2; GPR161

Cross-reactive species details

Due to limited amount of testing and knowledge, not every possible cross-reactivity is known.

Source

This antibody was obtained by immunization of the host with KLH conjugated synthetic peptide derived from human GPR161

Storage conditions

Store this antibody in aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Keep refrigerated at 2 to 8 degrees Celcius for up to one year.

Properties

For facs or microscopy Alexa 1 conjugate.Very high photo stable ALEXA conjugate.If you buy Antibodies supplied by Bioss Primary Conjugated Antibodies. ALEXA FLUOR they should be stored frozen at - 24°C for long term storage and for short term at + 5°C.

Background of the antigen

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).