PMID- 23055476
OWN - NLM
STAT- MEDLINE
DCOM- 20130103
LR  - 20220317
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 32
IP  - 41
DP  - 2012 Oct 10
TI  - Vps10 family proteins and the retromer complex in aging-related neurodegeneration 
      and diabetes.
PG  - 14080-6
LID - 10.1523/JNEUROSCI.3359-12.2012 [doi]
AB  - Members of the vacuolar protein sorting 10 (Vps10) family of receptors (including 
      sortilin, SorL1, SorCS1, SorCS2, and SorCS3) play pleiotropic functions in 
      protein trafficking and intracellular and intercellular signaling in neuronal and 
      non-neuronal cells. Interactions have been documented between Vps10 family 
      members and the retromer coat complex, a key component of the intracellular 
      trafficking apparatus that sorts cargo from the early endosome to the trans-Golgi 
      network. In recent years, genes encoding several members of the Vps10 family of 
      proteins, as well as components of the retromer coat complex, have been 
      implicated as genetic risk factors for sporadic and autosomal dominant forms of 
      neurodegenerative diseases, including Alzheimer's disease, frontotemporal lobar 
      degeneration, and Parkinson's disease, with risk for type 2 diabetes mellitus and 
      atherosclerosis. In addition to their functions in protein trafficking, the Vps10 
      family proteins modulate neurotrophic signaling pathways. Sortilin can impact the 
      intracellular response to brain-derived neurotrophic factor (BDNF) by regulating 
      anterograde trafficking of Trk receptors to the synapse and direct control of 
      BDNF levels, while both sortilin and SorCS2 function as cell surface receptors to 
      mediate acute responses to proneurotrophins. This mini-review and symposium will 
      highlight the emerging data from this rapidly growing area of research 
      implicating the Vps10 family of receptors and the retromer in physiological 
      intracellular trafficking signaling by neurotrophins and in the pathogenesis of 
      neurodegeneration.
FAU - Lane, Rachel F
AU  - Lane RF
AD  - Alzheimer's Drug Discovery Foundation, New York, New York 10019, USA. 
      RLane@alzdiscovery.org
FAU - St George-Hyslop, Peter
AU  - St George-Hyslop P
FAU - Hempstead, Barbara L
AU  - Hempstead BL
FAU - Small, Scott A
AU  - Small SA
FAU - Strittmatter, Stephen M
AU  - Strittmatter SM
FAU - Gandy, Sam
AU  - Gandy S
LA  - eng
GR  - P50 AG008702/AG/NIA NIH HHS/United States
GR  - CAPMC/CIHR/Canada
GR  - NS075685/NS/NINDS NIH HHS/United States
GR  - R01 NS074319/NS/NINDS NIH HHS/United States
GR  - P50 AG005138/AG/NIA NIH HHS/United States
GR  - NS074319/NS/NINDS NIH HHS/United States
GR  - Wellcome Trust/United Kingdom
GR  - NS030687/NS/NINDS NIH HHS/United States
GR  - 081864/Wellcome Trust/United Kingdom
GR  - R01 AG025161/AG/NIA NIH HHS/United States
GR  - AG034924/AG/NIA NIH HHS/United States
GR  - AG025161/AG/NIA NIH HHS/United States
GR  - R01 NS030687/NS/NINDS NIH HHS/United States
GR  - R01 AG034924/AG/NIA NIH HHS/United States
GR  - R01 NS075685/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (SORCS1 protein, human)
SB  - IM
MH  - Aging/genetics/*metabolism
MH  - Animals
MH  - Diabetes Mellitus, Type 2/genetics/*metabolism
MH  - Humans
MH  - Intracellular Space/physiology
MH  - Nerve Growth Factors/genetics/*physiology
MH  - Neural Pathways/pathology/physiology
MH  - Neurodegenerative Diseases/etiology/genetics/*metabolism
MH  - Protein Transport/genetics
MH  - Receptors, Cell Surface/genetics/*physiology
MH  - Signal Transduction/genetics
PMC - PMC3576841
MID - NIHMS414444
EDAT- 2012/10/12 06:00
MHDA- 2013/01/04 06:00
PMCR- 2013/04/10
CRDT- 2012/10/12 06:00
PHST- 2012/10/12 06:00 [entrez]
PHST- 2012/10/12 06:00 [pubmed]
PHST- 2013/01/04 06:00 [medline]
PHST- 2013/04/10 00:00 [pmc-release]
AID - 32/41/14080 [pii]
AID - 3805810 [pii]
AID - 10.1523/JNEUROSCI.3359-12.2012 [doi]
PST - ppublish
SO  - J Neurosci. 2012 Oct 10;32(41):14080-6. doi: 10.1523/JNEUROSCI.3359-12.2012.