What is he best known for?
The fields of study he is best known for:
His primary areas of study are Genetics, Locus, Missense mutation, Gene and Frameshift mutation.
His research in Mutation, Genetic linkage, Nonsyndromic deafness, Allele and Usher syndrome are components of Genetics.
His Locus research is multidisciplinary, incorporating perspectives in Hearing loss, Null allele and Exon.
His Missense mutation study incorporates themes from Consanguinity and Congenital cataracts.
His study in the field of Genetic heterogeneity, Transgene and Brown planthopper is also linked to topics like Stemborer.
His Frameshift mutation research is multidisciplinary, incorporating elements of Nonsense mutation, DNA sequencing and Candidate gene.
His most cited work include:
- Usher Syndrome 1D and Nonsyndromic Autosomal Recessive Deafness DFNB12 Are Caused by Allelic Mutations of the Novel Cadherin-Like Gene CDH23 (440 citations)
- Mutations in the gene encoding tight junction claudin-14 cause autosomal recessive deafness DFNB29. (367 citations)
- Mutations of the protocadherin gene PCDH15 cause Usher syndrome type 1F. (325 citations)
What are the main themes of his work throughout his whole career to date?
His scientific interests lie mostly in Genetics, Genetic linkage, Locus, Gene and Missense mutation.
His work is connected to Consanguinity, Mutation, Allele, Haplotype and Retinitis pigmentosa, as a part of Genetics.
Sheikh Riazuddin studied Mutation and Molecular biology that intersect with Mesenchymal stem cell.
His Genetic linkage research also works with subjects such as
- Genetic analysis most often made with reference to Congenital cataracts,
- Sanger sequencing and related Genetic heterogeneity.
His Locus research incorporates themes from Nonsyndromic deafness, Hearing loss, Lod score, Gene mapping and Exon.
His research investigates the connection between Missense mutation and topics such as Frameshift mutation that intersect with problems in Nonsense mutation.
He most often published in these fields:
- Genetics (94.51%)
- Genetic linkage (26.65%)
- Locus (18.96%)
What were the highlights of his more recent work (between 2016-2021)?
- Genetics (94.51%)
- Genetic linkage (26.65%)
- Mutation (23.63%)
In recent papers he was focusing on the following fields of study:
Genetics, Genetic linkage, Mutation, Intellectual disability and Exome sequencing are his primary areas of study.
Genetics is represented through his Microcephaly, Congenital cataracts, Disease gene identification, Allele and Retinitis pigmentosa research.
His Genetic linkage study integrates concerns from other disciplines, such as Sanger sequencing, Consanguinity, Genetic heterogeneity and Candidate gene.
Sheikh Riazuddin has included themes like Cataracts, Mutant protein and Locus in his Consanguinity study.
His Mutation research includes themes of Phenotype and Morphant.
His study looks at the intersection of Exome sequencing and topics like Retinal degeneration with Early onset, Cilium, Molecular biology and Intraflagellar transport.
Between 2016 and 2021, his most popular works were:
- Variants in PUS7 Cause Intellectual Disability with Speech Delay, Microcephaly, Short Stature, and Aggressive Behavior. (35 citations)
- Variants in PUS7 Cause Intellectual Disability with Speech Delay, Microcephaly, Short Stature, and Aggressive Behavior. (35 citations)
- Variants in PUS7 Cause Intellectual Disability with Speech Delay, Microcephaly, Short Stature, and Aggressive Behavior. (35 citations)
In his most recent research, the most cited papers focused on:
His primary areas of investigation include Genetics, Microcephaly, Intellectual disability, Mutation and Zebrafish.
His research links Ataxia with Genetics.
As a part of the same scientific family, Sheikh Riazuddin mostly works in the field of Microcephaly, focusing on Protein family and, on occasion, In silico, Frameshift mutation, Rab, Pontocerebellar hypoplasia and Cerebellum.
His biological study spans a wide range of topics, including Exon, Speech delay, Transfer RNA and Short stature.
His Disease gene identification research incorporates elements of Genetic analysis, Genetic linkage, Missense mutation and Candidate gene.
The concepts of his Locus study are interwoven with issues in Consanguinity, Genetic heterogeneity and Receptor tyrosine kinase, SPRY2.
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