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

NSD1 Rabbit anti-Human, Polyclonal, Invitrogen™

Rabbit Polyclonal Antibody

Manufacturer:  Invitrogen PA550857

Catalog No. PA550857


Add to cart

Description

Description

The antibody detects endogenous levels of total NSD1 / KMT3B protein.

This gene encodes a protein containing a SET domain, 2 LXXLL motifs, 3 nuclear translocation signals (NLSs), 4 plant homeodomain (PHD) finger regions, and a proline-rich region. The encoded protein enhances androgen receptor (AR) transactivation, and this enhancement can be increased further in the presence of other androgen receptor associated coregulators. This protein may act as a nucleus-localized, basic transcriptional factor and also as a bifunctional transcriptional regulator. Mutations of this gene have been associated with Sotos syndrome and Weaver syndrome. One version of childhood acute myeloid leukemia is the result of a cryptic translocation with the breakpoints occurring within nuclear receptor-binding Su-var, enhancer of zeste, and trithorax domain protein 1 on chromosome 5 and nucleoporin, 98-kd on chromosome 11. Two transcript variants encoding distinct isoforms have been identified for this gene.
Specifications

Specifications

NSD1
Polyclonal
Unconjugated
NSD1
Liquid
NSD1
Synthetic peptide of human nuclear receptor binding SET domain protein 1
Antigen affinity chromatography
RUO
Antibody
Polyclonal
Human
Immunohistochemistry (Paraffin)
1.5 mg/mL
PBS with 40% glycerol and 0.05% sodium azide; pH 7.4
Q96L73
ARA267, KMT3B
Rabbit
IgG
100 μL
-20°C
Primary
64324
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