alamut visual software v 2 6 1 (Sophia Genetics)
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alamut visual software v 2 6 1
Alamut Visual Software V 2 6 1, supplied by Sophia Genetics, used in various techniques. Bioz Stars score: 97/100, based on 1558 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/plus+software+v+1+6+1/Alamut+Visual+Plus/pm36535754-26-7-7
Average 97 stars, based on 1558 article reviews
Alamut Visual Software V 2 6 1, supplied by Sophia Genetics, used in various techniques. Bioz Stars score: 97/100, based on 1558 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/plus+software+v+1+6+1/Alamut+Visual+Plus/pm36535754-26-7-7
Average 97 stars, based on 1558 article reviews
alamut visual software v 2 6 1 - by Bioz Stars,
2026-09
97/100 stars
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Related Articles
Software:Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II Article Snippet: The variant NM_001042492.2:c.4174-679G > A ( a tgagatccttttttctttt AG gtccccaaga) does not alter the predicted strength of this acceptor site, however the branch point prediction integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II. Article Snippet: The variant NM_001042492.2:c.4174-679G > A (atgagatccttttttcttttAGgtccccaaga) does not alter the predicted strength of this acceptor site, however the branch point prediction integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II Article Snippet: In addition, the new branch points created by deep intronic variants were evaluated with the branch point prediction tool integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II Article Snippet: Namely, we evaluated the strength of all the wild-type splice sites, the de novo splice sites created by the variants and the cryptic splices sites activated by these variants using the following in-silico splicing predictions programs, i.e. NNSplice (v.0.9), MaxEntScan, SpliceSiteFinder-like and GeneSplicer, all embedded in Alamut Visual Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II. Article Snippet: In addition, the new branch points created by deep intronic variants were evaluated with the branch point prediction tool integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II. Article Snippet: Namely, we evaluated the strength of all the wild-type splice sites, the de novo splice sites created by the variants and the cryptic splices sites activated by these variants using the following in-silico splicing predictions programs, i.e. NNSplice (v.0.9), MaxEntScan, SpliceSiteFinder-like and GeneSplicer, all embedded in Alamut Visual Variant Assay:Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II Article Snippet: The variant NM_001042492.2:c.4174-679G > A ( a tgagatccttttttctttt AG gtccccaaga) does not alter the predicted strength of this acceptor site, however the branch point prediction integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II. Article Snippet: The variant NM_001042492.2:c.4174-679G > A (atgagatccttttttcttttAGgtccccaaga) does not alter the predicted strength of this acceptor site, however the branch point prediction integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II Article Snippet: In addition, the new branch points created by deep intronic variants were evaluated with the branch point prediction tool integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II Article Snippet: Namely, we evaluated the strength of all the wild-type splice sites, the de novo splice sites created by the variants and the cryptic splices sites activated by these variants using the following in-silico splicing predictions programs, i.e. NNSplice (v.0.9), MaxEntScan, SpliceSiteFinder-like and GeneSplicer, all embedded in Alamut Visual Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II. Article Snippet: In addition, the new branch points created by deep intronic variants were evaluated with the branch point prediction tool integrated in Article Title: Analysis of 200 unrelated individuals with a constitutional NF1 deep intronic pathogenic variant reveals that variants flanking the alternatively spliced NF1 exon 31 [23a] cause a classical neurofibromatosis type 1 phenotype while altering predominantly NF1 isoform type II. Article Snippet: Namely, we evaluated the strength of all the wild-type splice sites, the de novo splice sites created by the variants and the cryptic splices sites activated by these variants using the following in-silico splicing predictions programs, i.e. NNSplice (v.0.9), MaxEntScan, SpliceSiteFinder-like and GeneSplicer, all embedded in Alamut Visual |