High impact information on Fusip1

• The genes for neural-salient serine/arginine-rich (NSSR) proteins 1 and 2 have been cloned from the neuronal differentiated embryocarcinoma cell line, P19 [1].
• Cloning and characterization of two neural-salient serine/arginine-rich (NSSR) proteins involved in the regulation of alternative splicing in neurones [2].
• In contrast, transient transfection with NSSR 1 promotes the inclusion of the Flip exon so that the abnormal product is spliced to the mature spliced form [2].
• CONCLUSIONS: NSSR 1 and 2 were cloned from mouse cDNA libraries [2].
• RESULTS: We cloned two new SR proteins, Neural-salient SR proteins (NSSR) 1 and 2, which are present at higher levels in brain and testis [2].

Biological context of Fusip1

• Over-expression of NSSR 2 prevents the inclusion of either the Flip or Flop exons in the splicing of the GluR-B gene, resulting in an increase in the abnormal exon-skipping product [2].
• Immunohistostaining demonstrated that TASR-1 protein is more abundantly expressed than TASR-2 in mouse articular chondrocytes, raising the possibility that TASR-1 might be involved in phenotype maintenance of articular chondrocytes [3].

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 [3].
• In primarily cultured mouse neural progenitor cells (NPCs), at the undifferentiated status, NSSR1 transcripts were detected, but not the proteins [4].

Regulatory relationships of Fusip1

• The results demonstrate that NSSR1 promotes neuronal differentiation and the splicing of NCAML1 exon2 and TrkC-K1 [5].

Analytical, diagnostic and therapeutic context of Fusip1

• RT-PCR analysis revealed that TASR-1, but not TASR-2, influenced alternative splicing of type II and type XI collagens in ATDC5 cells [3].
• Results from our microarray analysis of ATDC5 cells showed that TASR-1 and TASR-2 differentially affect genes involved in the differentiation of chondrocytes [3].

References