Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

CRIM1 Rabbit anti-Human, Polyclonal, Invitrogen™

Rabbit Polyclonal Antibody

Manufacturer:  Invitrogen PA550643

Catalog No. PA550643


Add to cart

Description

Description

The antibody detects endogenous levels of total CRIM1 protein.

CRIM1 (cysteine-rich motor neuron 1), a glycosylated type I transmembrane protein, plays a role in tissue development i.e. capillary formation and maintece during angiogenesis. It contains an N-terminal IGF-binding protein-like motif and six von Willebrand-like cysteine-rich repeats (CRRs) in its extracellular domain. CRIM1 interacts with BMP4 and BMP7 via the CRRs and functions as an antagonist. CRIM1 is developmentally expressed in a number of tissues including the pancreas, kidney, placenta, brain and blood vessels. CRIM1 may participate in CNS and placental development by interacting with growth factors involved in motor neuron differentiation and survival.
Specifications

Specifications

CRIM1
Polyclonal
Unconjugated
CRIM1
Liquid
CRIM1
Synthetic peptide corresponding to a region derived from internal residues of human cysteine rich transmembrane BMP regulator 1 (chordin-like)
Antigen affinity chromatography
RUO
Antibody
Polyclonal
Human
Immunohistochemistry (Paraffin)
1.5 mg/mL
PBS with 50% glycerol and 0.05% sodium azide; pH 7.3
Q9NZV1
S52
Rabbit
IgG
100 μL
-20°C
Primary
51232
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit