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SRSF10  -  serine/arginine-rich splicing factor 10

Homo sapiens

Synonyms: 40 kDa SR-repressor protein, FUS-interacting serine-arginine-rich protein 1, FUSIP1, FUSIP2, NSSR, ...
 
 
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Disease relevance of FUSIP1

  • In vivo splicing assays indicated that SC35 and TASR influence splice site selection of adenovirus E1A pre-mRNA [1].
  • Our recent studies suggest that disruption of TASR-mediated pre-mRNA splicing is involved in the pathogenesis of human leukemia and sarcomas [2].
  • Characterization and expression of the human gene encoding two translocation liposarcoma protein-associated serine-arginine (TASR) proteins [2].
 

High impact information on FUSIP1

  • To investigate the cellular function of SRp38, we examined its possible role in cell cycle control [3].
  • The SR protein SRp38 represses splicing in M phase cells [3].
  • Using chimeric SRp38/SC35 proteins, we show that SC35-RBD/SRp38-RS can function as a general splicing activator and that the dephosphorylated version can act as a strong splicing repressor [4].
  • The SR protein SRp38 is a general splicing repressor that is activated by dephosphorylation during mitosis and in response to heat shock [4].
  • In transient-transfection assays, the TLS-ERG fusion protein inhibits E1A pre-mRNA splicing mediated by these TLS-associated SR proteins (TASR), and stable expression of the TLS-ERG fusion protein in K562 cells alters the splicing profile of CD44 mRNA [5].
 

Biological context of FUSIP1

  • The mRNA transcripts for TASR-1 and -2 share an identical sequence at the 5' untranslated region (5' UTR) and in part of the coding region; however the other regions of the transcripts diverge from each other and it was not clear whether the differences resulted from alternative splicing or transcription from two distinct genes [2].
  • Here we describe the assignment of both TASR cDNAs to the same 16 kb DNA segment located on chromosome 1 [2].
  • When cloned into a luciferase reporter and transfected into human cells, the TASR promoter construct generated luciferase activity that was at least 2000 fold greater than the promoterless plasmid [2].
  • In addition, multiple polyadenylation sites and a rare U12-type intron were found within the TASR gene [2].
  • Transcription initiation site of the TASR gene was determined by primer extension; analysis of the TASR promoter revealed that it lacks the TATA box but contains a GC-rich sequence [2].
 

Anatomical context of FUSIP1

  • Of special interest is the finding that TASR-1 could down-regulate expression of type X collagen, a hallmark of hypertrophic chondrocytes [6].
 

Associations of FUSIP1 with chemical compounds

  • The phosphatase inhibitor calyculin A prevented dephosphorylation of SRp38 during a heat shock and caused complete rephosphorylation of SRp38 after a heat shock, indicating that cells recovering from a heat shock are not deficient in kinase activity [7].
 

Physical interactions of FUSIP1

  • We further show that dephosphorylated SRp38 interacts with a U1 small nuclear ribonucleoprotein particle (snRNP) protein, and that this interaction interferes with 5'-splice-site recognition by the U1 snRNP [8].
 

Regulatory relationships of FUSIP1

  • Hsp27 enhances recovery of splicing as well as rephosphorylation of SRp38 after heat shock [7].
 

Other interactions of FUSIP1

  • Because of the similarity to SR proteins we have named these proteins SRrp40 and SRrp35, respectively, for SR-repressor proteins of approximately 40 and approximately 35 kDa [9].
  • The effect of Hsp27 on rephosphorylation of SRp38 required phosphorylatable Hsp27 [7].
  • Raising the Hsp70 level by either a pre-heat shock or by exogenous expression had no effect on either dephosphorylation of SRp38 during heat shock or rephosphorylation after heat shock [7].
  • A Hsp90 client protein was required for the effect of Hsp27 on recovery of spicing and on rephosphorylation of SRp38 [7].
 

Analytical, diagnostic and therapeutic context of FUSIP1

  • Northern blot analysis showed that at least five different TASR-1 and -2 transcripts are expressed in a broad range of human tissues [2].
  • RT-PCR analysis revealed that TASR-1, but not TASR-2, influenced alternative splicing of type II and type XI collagens in ATDC5 cells [6].
  • Results from our microarray analysis of ATDC5 cells showed that TASR-1 and TASR-2 differentially affect genes involved in the differentiation of chondrocytes [6].

References

  1. Oncoprotein TLS interacts with serine-arginine proteins involved in RNA splicing. Yang, L., Embree, L.J., Tsai, S., Hickstein, D.D. J. Biol. Chem. (1998) [Pubmed]
  2. Characterization and expression of the human gene encoding two translocation liposarcoma protein-associated serine-arginine (TASR) proteins. Clinton, J.M., Chansky, H.A., Odell, D.D., Zielinska-Kwiatkowska, A., Hickstein, D.D., Yang, L. Gene (2002) [Pubmed]
  3. The SR protein SRp38 represses splicing in M phase cells. Shin, C., Manley, J.L. Cell (2002) [Pubmed]
  4. Multiple properties of the splicing repressor SRp38 distinguish it from typical SR proteins. Shin, C., Kleiman, F.E., Manley, J.L. Mol. Cell. Biol. (2005) [Pubmed]
  5. TLS-ERG leukemia fusion protein inhibits RNA splicing mediated by serine-arginine proteins. Yang, L., Embree, L.J., Hickstein, D.D. Mol. Cell. Biol. (2000) [Pubmed]
  6. TASR-1 regulates alternative splicing of collagen genes in chondrogenic cells. Matsushita, H., Blackburn, M.L., Klineberg, E., Zielinska-Kwiatkowska, A., Bolander, M.E., Sarkar, G., Suva, L.J., Chansky, H.A., Yang, L. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
  7. Hsp27 enhances recovery of splicing as well as rephosphorylation of SRp38 after heat shock. Marin-Vinader, L., Shin, C., Onnekink, C., Manley, J.L., Lubsen, N.H. Mol. Biol. Cell (2006) [Pubmed]
  8. Dephosphorylated SRp38 acts as a splicing repressor in response to heat shock. Shin, C., Feng, Y., Manley, J.L. Nature (2004) [Pubmed]
  9. Serine-arginine (SR) protein-like factors that antagonize authentic SR proteins and regulate alternative splicing. Cowper, A.E., Cáceres, J.F., Mayeda, A., Screaton, G.R. J. Biol. Chem. (2001) [Pubmed]
 
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