Literature DB >> 8574969

Alzheimer-associated presenilins 1 and 2: neuronal expression in brain and localization to intracellular membranes in mammalian cells.

D M Kovacs1, H J Fausett, K J Page, T W Kim, R D Moir, D E Merriam, R D Hollister, O G Hallmark, R Mancini, K M Felsenstein, B T Hyman, R E Tanzi, W Wasco.   

Abstract

Mutations in two recently identified genes appear to cause the majority of early-onset familial Alzheimer's disease (FAD). These two novel genes, presenilin 1 (PS1) and presenilin 2 (PS2) are members of an evolutionarily conserved gene family. The normal biological role(s) of the presenilins and the mechanism(s) by which the FAD-associated mutations exert their effect remain unknown. Employing in situ hybridization, we demonstrate that the expression patterns of PS1 and PS2 in the brain are extremely similar to each other and that messages for both are primarily detectable in neuronal populations. Immunochemical analyses indicate that PS1 and PS2 are similar in size and localized to similar intracellular compartments (endoplasmic reticulum and Golgi complex). FAD-associated mutations in PS1 and PS2 do not significantly modify either their migration patterns on SDS-polyacrylamide gel electrophoresis or their overall subcellular localization, although subtle differences in perinuclear staining were noted for mutant PS1.

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Year:  1996        PMID: 8574969     DOI: 10.1038/nm0296-224

Source DB:  PubMed          Journal:  Nat Med        ISSN: 1078-8956            Impact factor:   53.440


  115 in total

Review 1.  Presenilins: structural aspects and posttranslational events.

Authors:  F Checler
Journal:  Mol Neurobiol       Date:  1999-06       Impact factor: 5.590

2.  C-terminal maturation fragments of presenilin 1 and 2 control secretion of APP alpha and A beta by human cells and are degraded by proteasome.

Authors:  C A da Costa; K Ancolio; F Checler
Journal:  Mol Med       Date:  1999-03       Impact factor: 6.354

Review 3.  The role of cell cycle-mediated events in Alzheimer's disease.

Authors:  A K Raina; M J Monteiro; A McShea; M A Smith
Journal:  Int J Exp Pathol       Date:  1999-04       Impact factor: 1.925

Review 4.  A genetic dichotomy model for the inheritance of Alzheimer's disease and common age-related disorders.

Authors:  R E Tanzi
Journal:  J Clin Invest       Date:  1999-11       Impact factor: 14.808

5.  Inhibition of intracellular cholesterol transport alters presenilin localization and amyloid precursor protein processing in neuronal cells.

Authors:  Heiko Runz; Jens Rietdorf; Inge Tomic; Marina de Bernard; Konrad Beyreuther; Rainer Pepperkok; Tobias Hartmann
Journal:  J Neurosci       Date:  2002-03-01       Impact factor: 6.167

6.  Interaction between amyloid precursor protein and presenilins in mammalian cells: implications for the pathogenesis of Alzheimer disease.

Authors:  W Xia; J Zhang; R Perez; E H Koo; D J Selkoe
Journal:  Proc Natl Acad Sci U S A       Date:  1997-07-22       Impact factor: 11.205

7.  Cell surface expression of the Alzheimer disease-related presenilin proteins.

Authors:  N N Dewji; S J Singer
Journal:  Proc Natl Acad Sci U S A       Date:  1997-09-02       Impact factor: 11.205

8.  Neuroinflammatory Cytokines-The Common Thread in Alzheimer's Pathogenesis.

Authors:  W Sue T Griffin; Steven W Barger
Journal:  US Neurol       Date:  2010

9.  Syntaxin 5 interacts with presenilin holoproteins, but not with their N- or C-terminal fragments, and affects beta-amyloid peptide production.

Authors:  Kei Suga; Takami Tomiyama; Hiroshi Mori; Kimio Akagawa
Journal:  Biochem J       Date:  2004-08-01       Impact factor: 3.857

10.  Age and sex dependent alteration in presenilin expression in mouse cerebral cortex.

Authors:  Mahendra Kumar Thakur; Soumi Ghosh
Journal:  Cell Mol Neurobiol       Date:  2007-09-15       Impact factor: 5.046

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