Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
The protein encoded by SNRPN is one polypeptide of a small nuclear ribonucleoprotein complex and belongs to the snRNP SMB/SMN family. Additionally we are shipping SNRPN Antibodies (70) and SNRPN Proteins (8) and many more products for this protein.
The androgenetic patterns of H19 (show NCKAP1 ELISA Kits), Snrpn, and Mest (show MEST ELISA Kits) were maintained even after differentiation of germline-derived pluripotent stem cells(gPS (show NBEAL2 ELISA Kits)) into neural stem cells(NSC), whereas the fully unmethylated status of Ndn (show NDN ELISA Kits) in SSCs was altered to somatic patterns in gPS (show NBEAL2 ELISA Kits) cells and gPS (show NBEAL2 ELISA Kits)-NSCs.
These data indicate that oocytes undergo time-dependent demethylation of Snrpn differentially methylated regions during the process of postovulatory aging.
Oocytes vitrification could lead to the loss of DNA methylation (show HELLS ELISA Kits) of imprinted genes (H19 (show NCKAP1 ELISA Kits), Peg3 (show PEG3 ELISA Kits), and Snrpn) in mouse blastocysts, which is mainly caused by the reductions of DNMTs after vitrification of oocytes.
These results support a model in which transcription from the Snrpn upstream exons directs the maternal imprint at the PWS-IC
Snrpn gene is imprinted, with monoallelic expression from the paternal allele in brain and heart.
the ATG-to-AAG mutation causes a 15-fold or more increase in translation of the downstream ORF in two fusion constructs, and it is likely that similar translational control affects the normal Snurf-Snrpn (show SNURF ELISA Kits) transcript as well
The tissue-specific methylation of the mouse conserved activator sequence and its methylation-sensitive enhancer activity may control expression of imprinting center transcripts, establishing and/or maintaining imprinting in the Snrpn locus.
Mouse model for Prader-Willi syndrome. Deletion of Snrpn gene and putative imprinting-centre is associated with absent expression of the imprinted genes Zfp127, Ndn a (show NDN ELISA Kits)nd Ipw, and phenotypes similar to those found in Prader-Willi infants.
we have confirmed that SNRPN methylation increases with age, which raises further questions regarding the role of SNRPN expression during the aging process.
the cases with partial loss of methylation in KCNQ1OT1 and SNRPN present clinical features different to those associated with the corresponding imprinting syndromes
Knockdown of SNRPN was demonstrated to significantly inhibit medulloblastoma cell growth and induce G2/M phase arrest in vitro.
indicate that SmN (show STMN1 ELISA Kits) expression reduces the level of mature U2 snRNP (show LSM2 ELISA Kits), leading to alternative splicing
The methylation patterns of the promoters of MTHFR (show MTHFR ELISA Kits) and SNRPN are associated with changes in sperm motility and morphology, which could lead to male infertility.
Human amniotic fluid mesenchymal stem cells contain a unique epigenetic signature during in vitro cell culture. H19 (show NCKAP1 ELISA Kits) and KCNQ1OT1 possessed a substantial degree of hypermethylation status, and variable DNA methylation (show HELLS ELISA Kits) patterns of SNRPN was observed.
In the skeletal muscle of neonate pigs, both NECD (show NDN ELISA Kits) and SNRPN were maternally imprinted, while UBE3A (show ube3a ELISA Kits) was not imprinted.
genetic association studies using 1,000 white subjects from Midwestern United States: Three copy number variations (CNV) in PWCR (show NDN ELISA Kits) are associated with body fat mass, with a higher copy number (CN) associated with an increase of in body fat mass.
Variable methylation of the imprinted gene, SNRPN, supports a relationship between intracranial germ cell tumours and neural stem cells.
SNRPN gene is imprinted, with monoallelic expression from the paternal allele in fetal brain and heart, and in adult brain.
SNRPN methylation profiles previously observed in mouse and human studies are also conserved in cattle
Results suggest that artificial reproductive techniques, such as prolonged in vitro culture and SCNT, lead to abnormal reprogramming of imprinting of SNRPN gene by altering methylation levels at this locus.
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.
sm protein D
, sm protein N
, small nuclear ribonucleoprotein-associated protein N
, tissue-specific-splicing protein
, SM protein N
, tissue-specific splicing protein
, FE294 gene for snRNP-associated polypeptide N
, FE294 psi pseudogene
, small nuclear ribonucleoparticle-associated protein (snRNP) mRNA clone Sm51
, small nuclear ribonucleoparticle-associated protein (snRNP) mRNA, clone Sm51
, small nuclear ribonucleoprotein N