File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The proNGF-p75NTR-sortilin signalling complex as new target for the therapeutic treatment of Parkinson's disease

TitleThe proNGF-p75NTR-sortilin signalling complex as new target for the therapeutic treatment of Parkinson's disease
Authors
KeywordsDeath signalling
Neurodegeneration
p75NTR
Parkinson's disease
ProNGF
Sortilin
Issue Date2008
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cdtcnsnd
Citation
Cns And Neurological Disorders - Drug Targets, 2008, v. 7 n. 6, p. 512-523 How to Cite?
AbstractGrowing evidence has shown that the p75 neurotrophin receptor (p75NTR) may play important roles in controlling neuronal survival or cell apoptosis within the central nervous system in development, and in pathological or neural injury. Recent studies have further revealed that p75NTR acts as a "molecular signal switch" that determines cell death or survival by three processes. First, pro-nerve growth factor (proNGF) triggers cell apoptosis by its high affinity binding to p75NTR, while NGF induces neuronal survival with low-affinity binding. Second, p75NTR mediates cell death by combining with co-receptor sortilin, whereas it promotes neuronal survival through combination with proNGF. Third, release of the intracellular domain chopper or cleavaged "short p75NTR" can independently initiate neuronal apoptosis. We have identified the cell self-destructive proNGF-p75NTR-sortilin signalling apparatus assembled in ventral tier dopamine neurons of the substantia nigra pars compacta, suggesting that p75NTR signalling might be involved in selective cell death mechanisms of substantia nigra neurons or disease progression of Parkinson's disease (PD). In addition, experimental manipulation of p75NTR benefited cell survival of cholinergic or motor neurons and improved disease progression of the neurodegenerative diseases Alzheimer's disease and Amyotrophic lateral sclerosis. The proNGF-p75NTR-sortilin signalling complex may thus provide new target for neuroprotection of substantia nigra neurons and the therapeutic treatment of PD. © 2008 Bentham Science Publishers Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/58283
ISSN
2015 Impact Factor: 2.188
2015 SCImago Journal Rankings: 0.883
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, LWen_HK
dc.contributor.authorYung, KKLen_HK
dc.contributor.authorChan, YSen_HK
dc.contributor.authorShum, DKYen_HK
dc.contributor.authorBolam, JPen_HK
dc.date.accessioned2010-05-31T03:27:24Z-
dc.date.available2010-05-31T03:27:24Z-
dc.date.issued2008en_HK
dc.identifier.citationCns And Neurological Disorders - Drug Targets, 2008, v. 7 n. 6, p. 512-523en_HK
dc.identifier.issn1871-5273en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58283-
dc.description.abstractGrowing evidence has shown that the p75 neurotrophin receptor (p75NTR) may play important roles in controlling neuronal survival or cell apoptosis within the central nervous system in development, and in pathological or neural injury. Recent studies have further revealed that p75NTR acts as a "molecular signal switch" that determines cell death or survival by three processes. First, pro-nerve growth factor (proNGF) triggers cell apoptosis by its high affinity binding to p75NTR, while NGF induces neuronal survival with low-affinity binding. Second, p75NTR mediates cell death by combining with co-receptor sortilin, whereas it promotes neuronal survival through combination with proNGF. Third, release of the intracellular domain chopper or cleavaged "short p75NTR" can independently initiate neuronal apoptosis. We have identified the cell self-destructive proNGF-p75NTR-sortilin signalling apparatus assembled in ventral tier dopamine neurons of the substantia nigra pars compacta, suggesting that p75NTR signalling might be involved in selective cell death mechanisms of substantia nigra neurons or disease progression of Parkinson's disease (PD). In addition, experimental manipulation of p75NTR benefited cell survival of cholinergic or motor neurons and improved disease progression of the neurodegenerative diseases Alzheimer's disease and Amyotrophic lateral sclerosis. The proNGF-p75NTR-sortilin signalling complex may thus provide new target for neuroprotection of substantia nigra neurons and the therapeutic treatment of PD. © 2008 Bentham Science Publishers Ltd.en_HK
dc.languageengen_HK
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/cdtcnsnden_HK
dc.relation.ispartofCNS and Neurological Disorders - Drug Targetsen_HK
dc.subjectDeath signallingen_HK
dc.subjectNeurodegenerationen_HK
dc.subjectp75NTRen_HK
dc.subjectParkinson's diseaseen_HK
dc.subjectProNGFen_HK
dc.subjectSortilinen_HK
dc.subject.meshAdaptor Proteins, Vesicular Transport - Metabolism - Physiology-
dc.subject.meshParkinson Disease - Drug Therapy - Metabolism-
dc.subject.meshNerve Growth Factor - Metabolism-
dc.subject.meshProtein Precursors - Metabolism-
dc.subject.meshDrug Delivery Systems - Methods - Trends-
dc.titleThe proNGF-p75NTR-sortilin signalling complex as new target for the therapeutic treatment of Parkinson's diseaseen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, YS: yschan@hkucc.hku.hken_HK
dc.identifier.emailShum, DKY: shumdkhk@hkucc.hku.hken_HK
dc.identifier.authorityChan, YS=rp00318en_HK
dc.identifier.authorityShum, DKY=rp00321en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2174/187152708787122923en_HK
dc.identifier.pmid19128208-
dc.identifier.scopuseid_2-s2.0-70350017843en_HK
dc.identifier.hkuros164132en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350017843&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue6en_HK
dc.identifier.spage512en_HK
dc.identifier.epage523en_HK
dc.identifier.isiWOS:000262654800003-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridChen, LW=7409444941en_HK
dc.identifier.scopusauthoridYung, KKL=13605496000en_HK
dc.identifier.scopusauthoridChan, YS=7403676627en_HK
dc.identifier.scopusauthoridShum, DKY=7004824447en_HK
dc.identifier.scopusauthoridBolam, JP=7004415425en_HK
dc.identifier.citeulike3865908-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats