SNRPN
Reactivité: Humain
WB, ELISA, IHC
Hôte: Lapin
Polyclonal
HRP
Indications d'application
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-2000,IHC 1:50-300
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
Liquid in PBS containing 50 % glycerol, 0.5 % BSA and 0.02 % sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
-20 °C
Stockage commentaire
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Date de péremption
12 months
Antigène
SNRPN
(Small Nuclear Ribonucleoprotein Polypeptide N (SNRPN))
Autre désignation
SNRPN
Sujet
SNRPN, HCERN3, SMN, Small nuclear ribonucleoprotein-associated protein N, snRNP-N, Sm protein D, Sm-D, Sm protein N, Sm-N, SmN, Tissue-specific-splicing proteinSmall nuclear ribonucleoprotein-associated protein N encoded by SNRPN is one polypeptide of a small nuclear ribonucleoprotein complex and belongs to the snRNP SMB/SMN family. The protein plays a role in pre-mRNA processing, possibly tissue-specific alternative splicing events. Although individual snRNPs are believed to recognize specific nucleic acid sequences through RNA-RNA base pairing, the specific role of this family member is unknown. The protein arises from a bicistronic transcript that also encodes a protein identified as the SNRPN upstream reading frame (SNURF). Multiple transcription initiation sites have been identified and extensive alternative splicing occurs in the 5' untranslated region. Additional splice variants have been described but sequences for the complete transcripts have not been determined. The 5' UTR of this gene has been identified as an imprinting center. Alternative splicing or deletion caused by a translocation event in this paternally-expressed region is responsible for Angelman syndrome or Prader-Willi syndrome due to parental imprint switch failure.