SYMPK

Symplekin
Rendering based on PDB 3O2Q.
Available structures PDB Ortholog search: PDBe, RCSB List of PDB id codes 3O2Q, 3O2S, 3O2T, 3ODR, 3ODS, 4H3H, 4H3K
Identifiers
Symbols	SYMPK; SPK; SYM
External IDs	OMIM: 602388 MGI: 1915438 HomoloGene: 37969 GeneCards: SYMPK Gene
Gene Ontology Molecular function • protein binding Cellular component • nucleus • nucleoplasm • nucleolus • cytoplasm • cytoskeleton • plasma membrane • tight junction Biological process • mRNA polyadenylation • cell adhesion • positive regulation of protein dephosphorylation Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	8189	68188
Ensembl	ENSG00000125755	ENSMUSG00000023118
UniProt	Q92797	Q80X82
RefSeq (mRNA)	NM_004819	NM_026605
RefSeq (protein)	NP_004810	NP_080881
Location (UCSC)	Chr 19: 46.32 – 46.37 Mb	Chr 7: 19.02 – 19.05 Mb
PubMed search
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Symplekin is a protein that in humans is encoded by the SYMPK gene.^[1][2] This gene encodes a nuclear protein that functions in the regulation of polyadenylation and promotes gene expression. The protein forms a high-molecular weight complex with components of the polyadenylation machinery. It is thought to serve as a scaffold for recruiting regulatory factors to the polyadenylation complex. It also participates in 3'-end maturation of histone mRNAs, which do not undergo polyadenylation. The protein also localizes to the cytoplasmic plaques of tight junctions in some cell types.^[2]

Model organisms

Model organisms have been used in the study of SYMPK function. A conditional knockout mouse line, called Sympk^{tm1a(EUCOMM)Wtsi[7][8]} was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.^[9][10][11]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.^[5][12] Twenty five tests were carried out on mutant mice and two significant abnormalities were observed.^[5] No homozygous mutant embryos were identified during gestation, and thus none survived until weaning. The remaining tests were carried out on heterozygous mutant adult mice; no additional significant abnormalities were observed in these animals.^[5]

Interactions

SYMPK has been shown to interact with CSTF2^[13] and HSF1.^[14]

References

Further reading