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

XRCC5 (Ku86) Mouse anti-Human, Unconjugated, Clone: N9C1, MilliporeSigma™

Mouse Monoclonal Antibody

Supplier:  MilliporeSigma MABE1892100UL

 View more versions of this product

Catalog No. MABE18921MI


Only null left
Add to Cart

Description

Description

XRCC5 (Ku86) Monoclonal antibody specifically detects XRCC5 (Ku86) in Human samples. It is validated for Western Blotting.
TRUSTED_SUSTAINABILITY
Specifications

Specifications

XRCC5 (Ku86)
Monoclonal
Unconjugated
X-ray repair cross-complementing protein 5;86 kDa subunit of Ku antigen;ATP-dependent DNA helicase 2 subunit 2;ATP-dependent DNA helicase II 80 kDa subunit;CTC box-binding factor 85 kDa subunit;CTC85;CTCBF;DNA repair protein XRCC5;Ku80;Ku86;Lupus Ku autoantigen protein p86;Nuclear factor IV;Thyroid-lupus autoantigen;TLAA;X-ray repair complementing defective repair in Chinese hamster cells 5
Mouse
∼80 kDa observed; 82.71 kDa calculated. Uncharacterized bands may be observed in some lysate(s).
100 μL
Primary
Human
Purified
Western Blot
N9C1
NP_066964
XRCC5, G22P2
Full-length human recombinant DNA repair protein XRCC5 (Ku86).
Protein G Purified
Epigenetics and Nuclear Function
Clone N9C1 is a mouse monoclonal antibody that specifically detects DNA repair protein XRCC5.
Stable for 1 year at 2 to 8°C from date of receipt.
IgG1 λ
Product Suggestions

Product Suggestions

Videos
SDS
Documents

Documents

Product Certifications
Promotions

Promotions

Product Content Correction

Your input is important to us. Please complete this form 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.