What is he best known for?
The fields of study he is best known for:
Ryszard Kole mostly deals with Molecular biology, RNA splicing, Oligonucleotide, Alternative splicing and Intron.
The Molecular biology study combines topics in areas such as Mutation, Morpholino and Exon.
Ryszard Kole works in the field of RNA splicing, focusing on Splice site mutation in particular.
His studies deal with areas such as Gel electrophoresis, Nucleic acid thermodynamics, Messenger RNA and Phosphodiester bond as well as Oligonucleotide.
His work focuses on many connections between Alternative splicing and other disciplines, such as Transfection, that overlap with his field of interest in Apoptosis.
His study in Intron is interdisciplinary in nature, drawing from both Gene expression and splice.
His most cited work include:
- Restoration of correct splicing in thalassemic pre-mRNA by antisense oligonucleotides. (329 citations)
- Systemically delivered antisense oligomers upregulate gene expression in mouse tissues (267 citations)
- Up-Regulation of Luciferase Gene Expression with Antisense Oligonucleotides: Implications and Applications in Functional Assay Development† (255 citations)
What are the main themes of his work throughout his whole career to date?
Ryszard Kole focuses on RNA splicing, Molecular biology, Oligonucleotide, Intron and Gene.
His work deals with themes such as splice and Messenger RNA, Alternative splicing, Exon, which intersect with RNA splicing.
His Alternative splicing research is multidisciplinary, incorporating perspectives in Apoptosis, Cancer research and Cancer.
His study looks at the relationship between Exon and topics such as Precursor mRNA, which overlap with Ribonucleoprotein.
Ryszard Kole interconnects Morpholino, Mutation, Transfection, HeLa and Globin in the investigation of issues within Molecular biology.
The concepts of his Oligonucleotide study are interwoven with issues in In vivo, Nucleic acid, Gene expression and RNase H.
He most often published in these fields:
- RNA splicing (62.75%)
- Molecular biology (54.90%)
- Oligonucleotide (31.37%)
What were the highlights of his more recent work (between 2007-2021)?
- RNA splicing (62.75%)
- Molecular biology (54.90%)
- Morpholino (15.69%)
In recent papers he was focusing on the following fields of study:
His primary scientific interests are in RNA splicing, Molecular biology, Morpholino, Cell biology and Exon skipping.
His RNA splicing study necessitates a more in-depth grasp of Gene.
Ryszard Kole has researched Molecular biology in several fields, including Oligonucleotide, DNA and Exon.
His work carried out in the field of Morpholino brings together such families of science as Deficient mouse, Pharmacology and Utrophin.
His Exon skipping research includes themes of Muscular dystrophy, Duchenne muscular dystrophy and Dystrophin.
His Messenger RNA research incorporates elements of Mutation and Intron.
Between 2007 and 2021, his most popular works were:
- Sustained dystrophin expression induced by peptide-conjugated morpholino oligomers in the muscles of mdx mice. (232 citations)
- Sustained dystrophin expression induced by peptide-conjugated morpholino oligomers in the muscles of mdx mice. (232 citations)
- Therapeutic potential of splice-switching oligonucleotides. (116 citations)
In his most recent research, the most cited papers focused on:
His primary areas of investigation include Molecular biology, Morpholino, Muscular dystrophy, Duchenne muscular dystrophy and Exon skipping.
His Molecular biology research incorporates themes from Thalassemia, Cardiac muscle, Mutation, Messenger RNA and splice.
His studies in Morpholino integrate themes in fields like mdx mouse, RNA splicing, Intron and Exon.
The study incorporates disciplines such as Regulator, Cancer, Cancer research and Downregulation and upregulation in addition to RNA splicing.
In general Muscular dystrophy, his work in Dystrophin is often linked to Diastole linking many areas of study.
His Duchenne muscular dystrophy research is multidisciplinary, incorporating elements of Endocrinology and Heart failure.
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