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B Pesold

Research Profile

Chemicals & Drugs

Disorders

Alzheimer's Disease

Anatomy

Cell Line

Physiology

Living Beings

Genes & Molecular Sequences

Amino Acid Sequences

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Publications

TOP 3
Kai Schönig; Tillmann Weber; Lena Wendler; Hermann Bujard; Dominik Djandji; Ariana Frömmig; B Pesold; Dusan Bartsch
Conditional gene expression systems in the transgenic rat brain.
Stefan M Berger; B Pesold; Simone Reber; Kai Schönig; Annette J Berger; Ina Weidenfeld; Jun Miao; Martin R Berger; Oliver J Gruss; Dusan Bartsch
Quantitative analysis of conditional gene inactivation using rationally designed, tetracycline-controlled miRNAs.
Johannes Thome; B Pesold; Miriam Baader; M Hu; Jonathan C Gewirtz; Ronald S Duman; Fritz A Henn
Stress differentially regulates synaptophysin and synaptotagmin expression in hippocampus.

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All Publications

2012: Kai Schönig; Tillmann Weber; Lena Wendler; Hermann Bujard; Dominik Djandji; Ariana Frömmig; B Pesold; Dusan Bartsch
Conditional gene expression systems in the transgenic rat brain.
BMC biology 2012;10():77.
2010: Stefan M Berger; B Pesold; Simone Reber; Kai Schönig; Annette J Berger; Ina Weidenfeld; Jun Miao; Martin R Berger; Oliver J Gruss; Dusan Bartsch
Quantitative analysis of conditional gene inactivation using rationally designed, tetracycline-controlled miRNAs.
Nucleic acids research 2010;38(17):e168.
2001: Johannes Thome; B Pesold; Miriam Baader; M Hu; Jonathan C Gewirtz; Ronald S Duman; Fritz A Henn
Stress differentially regulates synaptophysin and synaptotagmin expression in hippocampus.
Biological psychiatry 2001;50(10):809-12.
2001: Harald Steiner; Tamas Revesz; M Neumann; H Romig; MG Grim; B Pesold; Hans A Kretzschmar; John Hardy; Janice L Holton; Ralf Baumeister; Henry Houlden; Christian Haass
A pathogenic presenilin-1 deletion causes abberrant Abeta 42 production in the absence of congophilic amyloid plaques.
The Journal of biological chemistry 2001;276(10):7233-9.
2001: Johannes Thome; Wolfgang Retz; Miriam Baader; B Pesold; M Hu; M Cowen; Nuria Durany; Georg Adler; Fritz A Henn; Michael Rösler
Association analysis of HTR6 and HTR2A polymorphisms in sporadic Alzheimer's disease.
Journal of neural transmission (Vienna, Austria : 1996) 2001;108(10):1175-80.
2000: M Hu; Wolfgang Retz; Miriam Baader; B Pesold; Georg Adler; Fritz A Henn; Michael Rösler; Johannes Thome
Promoter polymorphism of the 5-HT transporter and Alzheimer's disease.
Neuroscience letters 2000;294(1):63-5.
2000: Harald Steiner; Marcus Kostka; H Romig; G Basset; B Pesold; John Hardy; Anja Capell; Liane Meyn; M L Grim; Ralf Baumeister; K Fechteler; Christian Haass
Glycine 384 is required for presenilin-1 function and is conserved in bacterial polytopic aspartyl proteases.
Nature cell biology 2000;2(11):848-51.
1999: Harald Steiner; B Pesold; Christian Haass
An in vivo assay for the identification of target proteases which cleave membrane-associated substrates.
FEBS letters 1999;463(3):245-9.
1999: Harald Steiner; H Romig; B Pesold; U Philipp; Miriam Baader; Martin Citron; Hansruedi Loetscher; Helmut Jacobsen; Christian Haass
Amyloidogenic function of the Alzheimer's disease-associated presenilin 1 in the absence of endoproteolysis.
Biochemistry 1999;38(44):14600-5.
1999: Harald Steiner; karen duff; Anja Capell; H Romig; MG Grim; Sarah J Lincoln; John Hardy; X Yu; M Picciano; K Fechteler; Martin Citron; R Kopan; B Pesold; S Keck; Miriam Baader; Taisuke Tomita; Takeshi Iwatsubo; Ralf Baumeister; Christian Haass
A loss of function mutation of presenilin-2 interferes with amyloid beta-peptide production and notch signaling.
The Journal of biological chemistry 1999;274(40):28669-73.
1999: Harald Steiner; H Romig; MG Grim; U Philipp; B Pesold; Martin Citron; Ralf Baumeister; Christian Haass
The biological and pathological function of the presenilin-1 Deltaexon 9 mutation is independent of its defect to undergo proteolytic processing.
The Journal of biological chemistry 1999;274(12):7615-8.
1998: Harald Steiner; Anja Capell; B Pesold; Martin Citron; P M Kloetzel; Dennis J Selkoe; H Romig; Klaus Mendla; Christian Haass
Expression of Alzheimer's disease-associated presenilin-1 is controlled by proteolytic degradation and complex formation.
The Journal of biological chemistry 1998;273(48):32322-31.
1998: Anja Capell; J Grünberg; B Pesold; A Diehlmann; Martin Citron; Ralph A. Nixon; Konrad Beyreuther; Dennis J Selkoe; Christian Haass
The proteolytic fragments of the Alzheimer's disease-associated presenilin-1 form heterodimers and occur as a 100-150-kDa molecular mass complex.
The Journal of biological chemistry 1998;273(6):3205-11.
1997: Jochen Walter; J Grünberg; Anja Capell; B Pesold; A Schindzielorz; Martin Citron; Klaus Mendla; Peter St George-Hyslop; Gerd Multhaup; Dennis J Selkoe; Christian Haass
Proteolytic processing of the Alzheimer disease-associated presenilin-1 generates an in vivo substrate for protein kinase C.
Proceedings of the National Academy of Sciences of the United States of America 1997;94(10):5349-54.
1996: Jochen Walter; Anja Capell; J Grünberg; B Pesold; A Schindzielorz; R Prior; Marcia B Podlisny; Paul E Fraser; Peter St George-Hyslop; Dennis J Selkoe; Christian Haass
The Alzheimer's disease-associated presenilins are differentially phosphorylated proteins located predominantly within the endoplasmic reticulum.
Molecular medicine (Cambridge, Mass.) 1996;2(6):673-91.