Role of RanBP9 on amyloidogenic processing of APP and synaptic protein levels in the mouse brain - Wikidata - wikimedia - TriplyDB

Role of RanBP9 on amyloidogenic processing of APP and synaptic protein levels in the mouse brain

Role of RanBP9 on amyloidogenic processing of APP and synaptic protein levels in the mouse brain

http://www.wikidata.org/entity/Q35913018

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Fragile X mental retardation protein controls synaptic vesicle exocytosis by modulating N-type calcium channel density Pivotal role of the RanBP9-cofilin pathway in Aβ-induced apoptosis and neurodegeneration.Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway.Cell signalling pathway regulation by RanBPM: molecular insights and disease implications.RanBP9 overexpression accelerates loss of dendritic spines in a mouse model of Alzheimer's disease COPS5 (Jab1) protein increases β site processing of amyloid precursor protein and amyloid β peptide generation by stabilizing RanBP9 protein levels.COPS5 protein overexpression increases amyloid plaque burden, decreases spinophilin-immunoreactive puncta, and exacerbates learning and memory deficits in the mouse brain Cooperative role of RanBP9 and P73 in mitochondria-mediated apoptosis.TFEB Overexpression in the P301S Model of Tauopathy Mitigates Increased PHF1 Levels and Lipofuscin Puncta and Rescues Memory Deficits.RanBP9 aggravates synaptic damage in the mouse brain and is inversely correlated to spinophilin levels in Alzheimer's brain synaptosomes RanBP9 overexpression accelerates loss of pre and postsynaptic proteins in the APΔE9 transgenic mouse brain.A lentiviral sponge for miR-101 regulates RanBP9 expression and amyloid precursor protein metabolism in hippocampal neurons.An AXL/LRP-1/RANBP9 complex mediates DC efferocytosis and antigen cross-presentation in vivo.RanBP9 overexpression reduces dendritic arbor and spine density.Targeting ApoE4/ApoE receptor LRP1 in Alzheimer's disease.Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.RanBP9 at the intersection between cofilin and Aβ pathologies: rescue of neurodegenerative changes by RanBP9 reduction Enhanced tau pathology via RanBP9 and Hsp90/Hsc70 chaperone complexes.

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Role of RanBP9 on amyloidogenic processing of APP and synaptic protein levels in the mouse brain

http://www.wikidata.org/entity/Q35913018

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

Role of RanBP9 on amyloidogeni ...... tein levels in the mouse brain

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Role of RanBP9 on amyloidogeni ...... tein levels in the mouse brain

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type

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Role of RanBP9 on amyloidogeni ...... tein levels in the mouse brain

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Role of RanBP9 on amyloidogeni ...... tein levels in the mouse brain

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prefLabel

Role of RanBP9 on amyloidogeni ...... tein levels in the mouse brain

@ast

Role of RanBP9 on amyloidogeni ...... tein levels in the mouse brain

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Role of RanBP9 on amyloidogeni ...... tein levels in the mouse brain

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Crystal D Hayes

http://www.w3.org/2001/XMLSchema#string

David E Kang

http://www.w3.org/2001/XMLSchema#string

Edward H Koo

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Elisabetta Bianchi

http://www.w3.org/2001/XMLSchema#string

Konda M Reddy

http://www.w3.org/2001/XMLSchema#string

Madepalli K Lakshmana

http://www.w3.org/2001/XMLSchema#string

Steven P Bennett

http://www.w3.org/2001/XMLSchema#string

P2860

RanBPM is an L1-interacting protein that regulates L1-mediated mitogen-activated protein kinase activation

The C terminus of fragile X mental retardation protein interacts with the multi-domain Ran-binding protein in the microtubule-organising centre

Proteolytic processing and cell biological functions of the amyloid precursor protein

Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase

Evidence that production and release of amyloid beta-protein involves the endocytic pathway

Disappearance of actin-binding protein, drebrin, from hippocampal synapses in Alzheimer's disease

Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment

Alzheimer's disease is a synaptic failure

RanBPM is a phosphoprotein that associates with the plasma membrane and interacts with the integrin LFA-1.

A fragment of the scaffolding protein RanBP9 is increased in Alzheimer's disease brains and strongly potentiates amyloid-beta peptide generation.

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2072-2083

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scholarly article

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10.1096/FJ.11-196709

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5

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26

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2012-01-31T00:00:00Z

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22294787

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3336780

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