|Application ||WB, IHC-P, E|
|Other Accession||P63164, P63163, Q60HD3, Q17QN3, NP_073716.1, NP_073717.1|
|Predicted||Bovine, Monkey, Mouse, Rat|
|Calculated MW||24614 Da|
|Antigen Region||34-62 aa|
|Other Names||Small nuclear ribonucleoprotein-associated protein N, snRNP-N, Sm protein D, Sm-D, Sm protein N, Sm-N, SmN, Tissue-specific-splicing protein, SNRPN, HCERN3, SMN|
|Target/Specificity||This SNRPN antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 34-62 amino acids from the N-terminal region of human SNRPN.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||SNRPN Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||May be involved in tissue-specific alternative RNA processing events.|
|Tissue Location||Expressed in brain and lymphoblasts.|
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Provided below are standard protocols that you may find useful for product applications.
The protein encoded by this gene 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.
Benetatos, L., et al. Leuk. Res. 34(2):148-153(2010)
Kim, S.J., et al. Am. J. Med. Genet. B Neuropsychiatr. Genet. 147B (7), 1116-1125 (2008) :
Horsthemke, B., et al. Am. J. Med. Genet. A 146A (16), 2041-2052 (2008) :
Runte, M., et al. Hum. Mol. Genet. 10(23):2687-2700(2001)
Kuslich, C.D., et al. Am. J. Hum. Genet. 64(1):70-76(1999)
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