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

PRRT2 Mouse anti-Human, Clone: OTI9H8, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA527223

Catalog No. PIMA527223


Add to cart

Description

Description

The proline-rich transmembrane protein 2 (PRRT2) contains a proline-rich domain in its N-terminal half and is predomitly expressed in brain and spinal cord in embryonic and postnatal stages. While little is known of the function of this protein, mutations in PRRT2 have been shown to be the causative gene of paroxysmal kinesigenic dyskinesia, which is characterized by recurrent, brief attacks of abnormal involuntary movements induced by sudden voluntary movements. Recent studies have shown that PRRT2 may also be involved in some forms of benign familial infantile epilepsy (BFIE), an autosomal domit epilepsy syndrome.
Specifications

Specifications

PRRT2
Monoclonal
1 mg/mL
PBS with 1% BSA, 50% glycerol and 0.02% sodium azide; pH 7.3
Q7Z6L0
PRRT2, Proline-rich transmembrane protein 2, dispanin subfamily B member 3, DSPB3, interferon induced transmembrane protein domain containing 1, IFITMD1, DYT10, EKD1
Mouse
IgG1
100 μL
-20° C, Avoid Freeze/Thaw Cycles
Primary
112476
Immunohistochemistry (Paraffin), Western Blot
OTI9H8
Unconjugated
PRRT2
Liquid
PRRT2
Human recombit protein fragment corresponding to amino acids 152-268 of PRRT2 produced in E.coli
Affinity Chromatography
RUO
Antibody
Monoclonal
Human
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