Literature DB >> 34453725

Assessing Rab5 Activation in Health and Disease.

Anna Pensalfini1, Ying Jiang2, Seonil Kim3, Ralph A Nixon2.   

Abstract

The endocytic pathway is a system of dynamically communicating vesicles, known as early endosomes, that internalize, sort, and traffic nutrients, trophic factors, and signaling molecules to sites throughout the cell. In all eukaryotic cells, early endosome functions are regulated by Rab5 activity, dependent upon its binding to GTP, whereas Rab5 bound to GDP represents the biologically inactive form. An increasing number of neurodegenerative diseases are associated with endocytic dysfunction and, in the case of Alzheimer's disease (AD) and Down syndrome (DS), an early appearing highly characteristic reflection of endocytic pathway dysfunction is an abnormal enlargement of Rab5 positive endosomes. In AD and DS, endosome enlargement accompanying accelerated endocytosis and fusion, upregulated transcription of endocytosis-related genes, and aberrant signaling by endosomes are caused by pathological Rab5 overactivation. In this chapter, we describe a battery of methods that have been used to assess Rab5 activation in models of AD/DS and are applicable to other cell and animal disease models. These methods include (1) fluorescence recovery after photobleaching (FRAP) assay; (2) quantitative measurement of endosome size by light, fluorescence and electron microscopy; (3) detection of GTP-Rab5 by in situ immunocytochemistry in vitro and ex vivo; (4) immunoprecipitation and GTP-agarose pull-down assay; (5) biochemical detection of Rab5 in endosome-enriched subcellular fractions obtained by OptiPrep™ density gradient centrifugation of mouse brain.
© 2021. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.

Entities:  

Keywords:  Alzheimer’s disease; Down syndrome; Endocytic dysfunction; Endocytosis; Endosomes; GDI; GTP-binding; Neurodegeneration; Rab5 activity

Mesh:

Substances:

Year:  2021        PMID: 34453725      PMCID: PMC8488988          DOI: 10.1007/978-1-0716-1346-7_20

Source DB:  PubMed          Journal:  Methods Mol Biol        ISSN: 1064-3745


  28 in total

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Journal:  Mol Cell Biol       Date:  2003-04       Impact factor: 4.272

2.  The small GTPase rab5 functions as a regulatory factor in the early endocytic pathway.

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Journal:  Cell       Date:  1992-09-04       Impact factor: 41.582

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Journal:  EMBO J       Date:  1997-02-03       Impact factor: 11.598

Review 4.  Endosome maturation.

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Journal:  EMBO J       Date:  2011-08-31       Impact factor: 11.598

Review 5.  Amyloid precursor protein and endosomal-lysosomal dysfunction in Alzheimer's disease: inseparable partners in a multifactorial disease.

Authors:  Ralph A Nixon
Journal:  FASEB J       Date:  2017-07       Impact factor: 5.191

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7.  App gene dosage modulates endosomal abnormalities of Alzheimer's disease in a segmental trisomy 16 mouse model of down syndrome.

Authors:  Anne M Cataldo; Suzana Petanceska; Corrinne M Peterhoff; Nicole B Terio; Charles J Epstein; Angela Villar; Elaine J Carlson; Matthias Staufenbiel; Ralph A Nixon
Journal:  J Neurosci       Date:  2003-07-30       Impact factor: 6.167

8.  Endosomal Dysfunction Induced by Directly Overactivating Rab5 Recapitulates Prodromal and Neurodegenerative Features of Alzheimer's Disease.

Authors:  Anna Pensalfini; Seonil Kim; Shivakumar Subbanna; Cynthia Bleiwas; Chris N Goulbourne; Philip H Stavrides; Ying Jiang; Ju-Hyun Lee; Sandipkumar Darji; Monika Pawlik; Chunfeng Huo; James Peddy; Martin J Berg; John F Smiley; Balapal S Basavarajappa; Ralph A Nixon
Journal:  Cell Rep       Date:  2020-11-24       Impact factor: 9.423

9.  Characterization of the early endosome and putative endocytic carrier vesicles in vivo and with an assay of vesicle fusion in vitro.

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Journal:  J Cell Biol       Date:  1989-04       Impact factor: 10.539

10.  APP processing is regulated by cytoplasmic phosphorylation.

Authors:  Ming-Sum Lee; Shih-Chu Kao; Cynthia A Lemere; Weiming Xia; Huang-Chun Tseng; Ying Zhou; Rachael Neve; Michael K Ahlijanian; Li-Huei Tsai
Journal:  J Cell Biol       Date:  2003-10-13       Impact factor: 10.539

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  1 in total

1.  The Alzheimer susceptibility gene BIN1 induces isoform-dependent neurotoxicity through early endosome defects.

Authors:  Erwan Lambert; Orthis Saha; Marcos R Costa; Pierre Dourlen; Bruna Soares Landeira; Ana Raquel Melo de Farias; Xavier Hermant; Arnaud Carrier; Alexandre Pelletier; Johanna Gadaut; Lindsay Davoine; Cloé Dupont; Philippe Amouyel; Amélie Bonnefond; Frank Lafont; Farida Abdelfettah; Patrik Verstreken; Julien Chapuis; Nicolas Barois; Fabien Delahaye; Bart Dermaut; Jean-Charles Lambert
Journal:  Acta Neuropathol Commun       Date:  2022-01-08       Impact factor: 7.801

  1 in total

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