His main research concerns Genetics, Molecular biology, Gene, Mutation and Amyotrophic lateral sclerosis. His studies in Gene duplication, Exon, Missense mutation, Genetic linkage and Gene mapping are all subfields of Genetics research. His Molecular biology research incorporates themes from Cell culture, Multiple drug resistance, Cancer research, Nucleic acid and Multidrug resistance-associated protein 2.
His Multiple drug resistance study combines topics from a wide range of disciplines, such as Daunorubicin and Cell. His Mutation study combines topics in areas such as Splice site mutation, Endocrinology and Internal medicine, Hypoplasia. His Amyotrophic lateral sclerosis research includes themes of Genome-wide association study, Exome, Haplotype and Case-control study.
His scientific interests lie mostly in Genetics, Gene, Immunology, Molecular biology and Pathology. Mutation, Exon, Missense mutation, Allele and Gene duplication are subfields of Genetics in which his conducts study. Frank Baas works on Mutation which deals in particular with Pontocerebellar hypoplasia.
His Gene study frequently links to other fields, such as Internal medicine. Immunology is closely attributed to breakpoint cluster region in his study. The study incorporates disciplines such as Cell culture and P-glycoprotein, Multiple drug resistance in addition to Molecular biology.
Frank Baas mostly deals with Genetics, Immunology, Gene, Pathology and Mutation. In most of his Genetics studies, his work intersects topics such as Neurodegeneration. Frank Baas studied Immunology and breakpoint cluster region that intersect with B-cell receptor, Prospective cohort study, Autoantibody and Rituximab.
His research investigates the connection with Gene and areas like Molecular biology which intersect with concerns in Cell culture. Frank Baas is involved in the study of Pathology that focuses on Amyotrophic lateral sclerosis in particular. His work in Mutation tackles topics such as Exon which are related to areas like Compound heterozygosity.
Frank Baas spends much of his time researching Genetics, Gene, Mutation, Amyotrophic lateral sclerosis and Missense mutation. Genetics is closely attributed to Neurodegeneration in his work. His Gene research includes elements of Transport protein, Annexin and Protein aggregation.
His Mutation research incorporates themes from Medical genetics, Case-control study, Risk factor and Genomics. His Pathology study integrates concerns from other disciplines, such as Immunology and Trinucleotide repeat expansion. Frank Baas works mostly in the field of Cell biology, limiting it down to topics relating to Enhancer and, in certain cases, Molecular biology, as a part of the same area of interest.
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Analysis of expression of cMOAT (MRP2), MRP3, MRP4, and MRP5, homologues of the multidrug resistance-associated protein gene (MRP1), in human cancer cell lines.
M. Kool;M. De Haas;G. L. Scheffer;R. J. Scheper.
Cancer Research (1997)
The Human Transcriptome Map: Clustering of Highly Expressed Genes in Chromosomal Domains
Huib Caron;Barbera van Schaik;Merlijn van der Mee;Frank Baas.
Science (2001)
The human multidrug resistance-associated protein MRP is a plasma membrane drug-efflux pump.
G.J.R. Zaman;M.J. Flens;M.R. van Leusden;M. de Haas.
Proceedings of the National Academy of Sciences of the United States of America (1994)
Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways
Elizabeth T. Cirulli;Brittany N Lasseigne;Slave Petrovski;Peter C Sapp.
Science (2015)
Duplication in chromosome 17p11.2 in Charcot-Marie-Tooth neuropathy type 1a (CMT 1a). The HMSN Collaborative Research Group.
P Raeymaekers;V Timmerman;E Nelis;P De Jonghe.
Neuromuscular Disorders (1991)
MRP3, an organic anion transporter able to transport anti-cancer drugs
M. Kool;M. van der Linden;M. de Haas;G. L. Scheffer.
Proceedings of the National Academy of Sciences of the United States of America (1999)
Identification of mutations in the gene encoding lamins A/C in autosomal dominant limb girdle muscular dystrophy with atrioventricular conduction disturbances (LGMD1B)
Muchir A;Bonne G;van der Kooi Aj;van Meegen M.
Human Molecular Genetics (2000)
A mutation in the human canalicular multispecific organic anion transporter gene causes the Dubin-Johnson syndrome.
C. C. Paulusma;M. Kool;P. J. Bosma;G. L. Scheffer.
Hepatology (1997)
Mutations in ABCC6 cause pseudoxanthoma elasticum.
A.A. Bergen;A.S. Plomp;E.J. Schuurman;S. Terry.
Nature Genetics (2000)
Role of glutathione in the export of compounds from cells by the multidrug-resistance-associated protein
G J Zaman;J Lankelma;O van Tellingen;J Beijnen.
Proceedings of the National Academy of Sciences of the United States of America (1995)
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