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Pre-mRNA splicing occurs in 2 sequential transesterification steps. 再加上，我们可以发 和 和数多这个蛋白质的别的产品。
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Within early haematopoiesis, myeloid differentiation is impaired, suggesting Prpf8 is required for haematopoietic development.
Multiple genes contributing to the retinal dystrophy (显示 MERTK 抗体) genotypes within a family were discovered using retinal gene-targeted next-generation sequencing. Families with noted examples of phenotypic variation or apparent non-penetrant individuals may offer a clue to suspect complex inheritance.
Frame-shift mutations and nonconservative amino acid changes in PRPF8 typically cause severe clinical phenotypes. The conservative missense variant p.PRPF8-Arg2310Lys that is not altering the global charge of the C-terminal tail, and variants located at the basis of the C-terminal tail show milder clinical phenotypes, in accordance with functional data on PRPF8/SNRNP200 (显示 SNRNP200 抗体) interactions in yeast.
We show that PRP31 (显示 PRPF31 抗体), a component of U4 snRNP (显示 LSM2 抗体), is modified with K63-linked ubiquitin chains by the PRP19 (显示 PRPF19 抗体) complex and deubiquitinated by USP15 (显示 USP15 抗体) and its substrate targeting factor SART3 (显示 SART3 抗体). USP15SART3 makes a complex with USP4 (显示 USP4 抗体) and this ternary complex serves as a platform to deubiquitinate PRP31 (显示 PRPF31 抗体) and PRP3 (显示 CLCA4 抗体)
HSP90 (显示 HSP90 抗体)/R2TP chaperone system promotes the assembly of a key module of U5 snRNP (显示 LSM2 抗体) while assuring the quality control of PRPF8. The proteomics data further reveal new interactions between R2TP and the tuberous sclerosis complex, pointing to a potential link between growth signals and the assembly of key cellular machines.
influenza A virus upregulates cellular PRPF8 gene expression through viral NS1 protein and influenza virus polymerase basic protein 1 to increase virus production.
Our findings exemplify the regulatory potential of changes in the core spliceosome machinery, which may be relevant to slow-onset human genetic diseases linked to PRPF8 deficiency
Most importantly between Prp8 and nucleotides at the exon-intron junction.
A mutation in a splicing factor (显示 SLU7 抗体) PRPF8 that causes retinitis pigmentosa has a transcriptome-wide effect on mRNA splicing.
Data suggest Enterovirus 3DPol (RNA-dependent RNA polymerase) enters nucleus via nuclear localization signal, targets pre-mRNA processing factor 8 (Prp8) to block pre-mRNA splicing/mRNA synthesis, and shuts off cellular transcription/translation.
In the cytoplasm, Prp8 forms a precursor complex with U5 snRNA
The mouse retinal pigment epithelium (RPE (显示 RPE 抗体))is the primary cell affected by mutations in the RNA splicing factors (PRPF3 (显示 PRPF3 抗体), PRPF8, and PRPF31 (显示 PRPF31 抗体)), and these changes occur at an early age.
found that PRP31 (显示 PRPF31 抗体) and PRPC8 as well as snRNAs are highly expressed in retinal cells
The finding of similar degenerative changes in RPE (显示 RPE 抗体) cells of all three mouse models suggests that the retinal pigment epithelium may be the primary cell type affected in the RNA splicing factor (显示 SLU7 抗体) forms of retinitis pigmentosa.
Pre-mRNA splicing occurs in 2 sequential transesterification steps. The protein encoded by this gene is a component of both U2- and U12-dependent spliceosomes, and found to be essential for the catalytic step II in pre-mRNA splicing process. It contains several WD repeats, which function in protein-protein interactions. This protein has a sequence similarity to yeast Prp8 protein. This gene is a candidate gene for autosomal dominant retinitis pigmentosa.
PRP8 pre-mRNA processing factor 8 homolog
, pre-mRNA-processing-splicing factor 8
, 220 kDa U5 snRNP-specific protein
, PRP8 homolog
, U5 snRNP-specific protein (220 kD), ortholog of S. cerevisiae Prp8p
, apoptosis-regulated protein 1
, apoptosis-regulated protein 2
, precursor mRNA processing protein
, splicing factor Prp8