D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 61 Citations 11,262 141 World Ranking 7543 National Ranking 559

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • Amino acid

The scientist’s investigation covers issues in Biochemistry, Formylglycine-generating enzyme, Cell biology, Cysteine and Peptide sequence. He merges Biochemistry with Fluorescence spectroscopy in his research. Bernhard Schmidt interconnects Multiple sulfatase deficiency, Gene and Active site in the investigation of issues within Formylglycine-generating enzyme.

His work carried out in the field of Cell biology brings together such families of science as Tyrosine, Lysosome, Endocytosis and Lysosomal acid phosphatase, Acid phosphatase. His Peptide sequence study integrates concerns from other disciplines, such as Amino acid and Complementary DNA. His Arylsulfatase study combines topics from a wide range of disciplines, such as Molecular biology and Arylsulfatase A.

His most cited work include:

  • Role of microglia and host prion protein in neurotoxicity of a prion protein fragment (468 citations)
  • Prion protein-deficient cells show altered response to oxidative stress due to decreased SOD-1 activity (392 citations)
  • Multiple Sulfatase Deficiency Is Caused by Mutations in the Gene Encoding the Human Cα-Formylglycine Generating Enzyme (317 citations)

What are the main themes of his work throughout his whole career to date?

His primary areas of investigation include Biochemistry, Molecular biology, Formylglycine-generating enzyme, Cell biology and Sulfatase. Peptide sequence, Multiple sulfatase deficiency, Endoplasmic reticulum, Mannose and Amino acid are the subjects of his Biochemistry studies. His Molecular biology research incorporates elements of RNA, Wild type, Cathepsin H and Arylsulfatase A.

His Formylglycine-generating enzyme research includes elements of Residue, Aldehyde, Arylsulfatase and Active site. His research investigates the connection between Cell biology and topics such as Endocytosis that intersect with issues in Acid phosphatase and Lysosomal acid phosphatase. His research in Cysteine intersects with topics in Conserved sequence and Serine.

He most often published in these fields:

  • Biochemistry (61.59%)
  • Molecular biology (22.52%)
  • Formylglycine-generating enzyme (22.52%)

What were the highlights of his more recent work (between 2008-2019)?

  • Biochemistry (61.59%)
  • Cell biology (16.56%)
  • Multiple sulfatase deficiency (13.25%)

In recent papers he was focusing on the following fields of study:

Bernhard Schmidt mainly focuses on Biochemistry, Cell biology, Multiple sulfatase deficiency, Formylglycine-generating enzyme and Sulfatase. As part of the same scientific family, Bernhard Schmidt usually focuses on Cell biology, concentrating on Transmembrane protein and intersecting with Integral membrane protein, Vesicle-associated membrane protein 8, Peptide sequence and Membrane protein. Bernhard Schmidt has included themes like Internal medicine, Protein disulfide-isomerase and Endocrinology in his Multiple sulfatase deficiency study.

His Formylglycine-generating enzyme research is multidisciplinary, incorporating perspectives in Secretory protein and Endoplasmic reticulum. His Endoplasmic reticulum research incorporates themes from Secretion, Cysteine and Furin. His study focuses on the intersection of SUMF1 Gene and fields such as Compound heterozygosity with connections in the field of Molecular biology.

Between 2008 and 2019, his most popular works were:

  • Molecular basis of multiple sulfatase deficiency, mucolipidosis II/III and Niemann-Pick C1 disease — Lysosomal storage disorders caused by defects of non-lysosomal proteins☆ (74 citations)
  • Tim50’s presequence receptor domain is essential for signal driven transport across the TIM23 complex (69 citations)
  • SUMF1 mutations affecting stability and activity of formylglycine generating enzyme predict clinical outcome in multiple sulfatase deficiency (43 citations)

In his most recent research, the most cited papers focused on:

  • Enzyme
  • Gene
  • Amino acid

Bernhard Schmidt spends much of his time researching Cell biology, Translocase of the inner membrane, Biochemistry, Mitochondrial membrane transport protein and TIM/TOM complex. He has researched Cell biology in several fields, including RNA, RNA Helicase A and Helicase. Bernhard Schmidt has included themes like Saccharomyces cerevisiae and Inner membrane in his Translocase of the inner membrane study.

In his works, he conducts interdisciplinary research on Biochemistry and Niemann–Pick disease, type C. His work in the fields of Mitochondrial membrane transport protein, such as Translocase of the outer membrane, overlaps with other areas such as Intermembrane space. He combines subjects such as Isoelectric point, Phosphatase, Dephosphorylation and Lysosomal acid phosphatase, Acid phosphatase with his study of Mannose 6-phosphate receptor.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Role of microglia and host prion protein in neurotoxicity of a prion protein fragment

David R. Brown;Bernhard Schmidt;Hans A. Kretzschmar.
Nature (1996)

633 Citations

Prion protein-deficient cells show altered response to oxidative stress due to decreased SOD-1 activity

David R. Brown;Walter J. Schulz-Schaeffer;Bernhard Schmidt;Hans A. Kretzschmar.
Experimental Neurology (1997)

585 Citations

A Novel Amino Acid Modification in Sulfatases That Is Defective in Multiple Sulfatase Deficiency

Bernhard Schmidt;Thorsten Selmer;Arnd Ingendoh;Kurt von Figurat.
Cell (1995)

480 Citations

Multiple Sulfatase Deficiency Is Caused by Mutations in the Gene Encoding the Human Cα-Formylglycine Generating Enzyme

Thomas Dierks;Bernhard Schmidt;Ljudmila V. Borissenko;Jianhe Peng.
Cell (2003)

393 Citations

Phosphorylation of microtubule-associated protein tau: identification of the site for Ca2(+)-calmodulin dependent kinase and relationship with tau phosphorylation in Alzheimer tangles.

B. Steiner;E. M. Mandelkow;J. Biernat;N. Gustke.
The EMBO Journal (1990)

393 Citations

Prion Protein Binds Copper within the Physiological Concentration Range

Michael L. Kramer;Hartmut D. D. Kratzin;Bernhard Schmidt;Alice Römer.
Journal of Biological Chemistry (2001)

332 Citations

The race-specific elicitor, NIP1, from the barley pathogen, Rhynchosporium secalis, determines avirulence on host plants of the Rrs1 resistance genotype.

M Rohe;A Gierlich;H Hermann;M Hahn.
The EMBO Journal (1995)

276 Citations

Highly conserved and disease‐specific patterns of carboxyterminally truncated Aβ peptides 1–37/38/39 in addition to 1–40/42 in Alzheimer's disease and in patients with chronic neuroinflammation

J. Wiltfang;H. Esselmann;M. Bibl;A. Smirnov.
Journal of Neurochemistry (2002)

261 Citations

Targeting of a lysosomal membrane protein: a tyrosine-containing endocytosis signal in the cytoplasmic tail of lysosomal acid phosphatase is necessary and sufficient for targeting to lysosomes.

C Peters;M Braun;B Weber;M Wendland.
The EMBO Journal (1990)

248 Citations

Guanidinoacetate methyltransferase deficiency: the first inborn error of creatine metabolism in man.

S. Stöckler;D. Isbrandt;F. Hanefeld;B. Schmidt.
American Journal of Human Genetics (1996)

241 Citations

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