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

TXNL6 Rabbit anti-Human, Mouse, Polyclonal, Proteintech
SDP

Rabbit Polyclonal Antibody

Supplier:  Proteintech Group Inc 112031AP150UL

Encompass_Preferred

 View more versions of this product

Catalog No. 50-172-6966


May include imposed supplier surcharges.
Only null left
Add to Cart

Description

Description

Retinitis pigmentosa (RP) is a disease that leads to blindness by degeneration of cone photoreceptors. Rods produce factors required for cone viability. The protein encoded by this gene is one of those factors and is similar to a truncated form of thioredoxin. This gene has been proposed to have therapeutic value against RP.
Specifications

Specifications

TXNL6
Polyclonal
Unconjugated
NXNL1
nucleoredoxin like 1, Nucleoredoxin like protein 1, NXNL1, RDCVF, Thioredoxin like protein 6, TXNL6
Rabbit
Antigen Affinity Chromatography
RUO
115861, 234404
-20°C
Liquid
Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blot
0.27 mg/mL
PBS with 50% glycerol and 0.1% sodium azide; pH 7.3
Q8VC33, Q96CM4
Nxnl1
TXNL6 Fusion Protein Ag1691
150 μL
Primary
Human, Mouse
Antibody
IgG
Product Suggestions

Product Suggestions

Videos
SDS
Documents

Documents

Product Certifications
Promotions

Promotions

Product Content Correction

The Fisher Scientific Encompass Program offers items which are not part of our distribution portfolio. These products typically do not have pictures or detailed descriptions. However, we are committed to improving your shopping experience. 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.

Your feedback has been submitted: Thank you for helping us improve our website.