hnRNP K polyclonal, anti-human, mouse, rat
€470.00
In stock
SKU
AC-AP70385
Background:
One of the major pre-mRNA-binding proteins. Binds tenaciously to poly(C) sequences. Likely to play a role in the nuclear metabolism of hnRNAs, particularly for pre-mRNAs that contain cytidine-rich sequences. Can also bind poly(C) single- stranded DNA. Plays an important role in p53/TP53 response to DNA damage, acting at the level of both transcription activation and repression. When sumoylated, acts as a transcriptional coactivator of p53/TP53, playing a role in p21/CDKN1A and 14-3-3 sigma/SFN induction (By similarity). As far as transcription repression is concerned, acts by interacting with long intergenic RNA p21 (lincRNA-p21), a non-coding RNA induced by p53/TP53. This interaction is necessary for the induction of apoptosis, but not cell cycle arrest.
Other Names:
HNRNPK; HNRPK; Heterogeneous nuclear ribonucleoprotein K; hnRNP K; Transformation up-regulated nuclear protein; TUNP
Antigen Type: synthetic peptide
Antigen Type: HNRNPK
Gene ID: 3190
Primary Accession: P61978
One of the major pre-mRNA-binding proteins. Binds tenaciously to poly(C) sequences. Likely to play a role in the nuclear metabolism of hnRNAs, particularly for pre-mRNAs that contain cytidine-rich sequences. Can also bind poly(C) single- stranded DNA. Plays an important role in p53/TP53 response to DNA damage, acting at the level of both transcription activation and repression. When sumoylated, acts as a transcriptional coactivator of p53/TP53, playing a role in p21/CDKN1A and 14-3-3 sigma/SFN induction (By similarity). As far as transcription repression is concerned, acts by interacting with long intergenic RNA p21 (lincRNA-p21), a non-coding RNA induced by p53/TP53. This interaction is necessary for the induction of apoptosis, but not cell cycle arrest.
Other Names:
HNRNPK; HNRPK; Heterogeneous nuclear ribonucleoprotein K; hnRNP K; Transformation up-regulated nuclear protein; TUNP
Antigen Type: synthetic peptide
Antigen Type: HNRNPK
Gene ID: 3190
Primary Accession: P61978
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