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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Stathmin-like 2

regulatory phosphoprotein; involved in promoting microtubule depolymerization and maintenance of long-term synaptic plasticity [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Stathmin, GAP-43, GAP, CAN, NGF
Papers on SCG10
Proximity of SCG10 and prion protein in membrane rafts.
Yokoyama et al., Tsukuba, Japan. In J Neurochem, Jan 2016
Liquid chromatography-tandem mass spectrometry analysis resulted in the identification of peptides containing SCG10, the neuron-specific microtubule regulator.
Spy1 Protein Mediates Phosphorylation and Degradation of SCG10 Protein in Axonal Degeneration.
Shen et al., Nantong, China. In J Biol Chem, Jun 2015
Recent data demonstrate that SCG10 is a novel axonal maintenance factor and that rapid SCG10 loss after injury requires JNK activity; how JNK induces degradation of SCG10 is not well known.
Intervention with 7,8-dihydroxyflavone blocks further striatal terminal loss and restores motor deficits in a progressive mouse model of Parkinson's disease.
Meshul et al., Portland, United States. In Neuroscience, May 2015
Animals treated with MPTP and 7,8-DHF also demonstrated increased levels of, a sprouting-associated protein, superior cervical ganglion-10 (SCG10), phosphorylated TrkB (pTrkB), and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) within the DL striatum and substantia nigra (SN) compared to the 4-week MPTP-treated animals.
In vitro screen of prion disease susceptibility genes using the scrapie cell assay.
Lloyd et al., London, United Kingdom. In Hum Mol Genet, 2014
While no consistent differences were determined for seven genes, highly significant changes were detected for Zbtb38, Sorcs1, Stmn2, Hspa13, Fkbp9, Actr10 and Plg, suggesting that they play key roles in the fundamental processes of prion propagation or clearance.
Comparative gene array analysis of progenitor cells from human paired deep neck and subcutaneous adipose tissue.
Wabitsch et al., Ulm, Germany. In Mol Cell Endocrinol, 2014
Analysis of highest regulated genes revealed that STMN2, MME, ODZ2, NRN1 and IL13RA2 genes were specifically expressed in white progenitor cells, whereas expression of LRRC17, CNTNAP3, CD34, RGS7BP and ADH1B marked brown progenitor cells.
Functional and molecular defects of hiPSC-derived neurons from patients with ATM deficiency.
Delia et al., Milano, Italy. In Cell Death Dis, 2013
We show that A-T neurons display similar voltage-gated potassium and sodium currents and discharges of action potentials as control neurons, but defective expression of the maturation and synaptic markers SCG10, SYP and PSD95 (postsynaptic density protein 95).
Dynamic expression of Notch-dependent neurogenic markers in the chick embryonic nervous system.
Dupé et al., Rennes, France. In Front Neuroanat, 2013
Their temporal and spatial expression were compared with the neuronal markers Nescient Helix-Loop-Helix 1 (Nhlh1), Stathmin 2 (Stmn2) and HuC/D.
Gene expression profiling in the pituitary gland of laying period and ceased period huoyan geese.
Zhang et al., Shenyang, China. In Asian-australas J Anim Sci, 2013
Among these genes, Synaptotagmin-1 (SYT1) and Stathmin-2 (STMN2) were substantially over-expressed in laying period compared to ceased period.
Genetics of prion diseases.
Collinge et al., London, United Kingdom. In Curr Opin Genet Dev, 2013
Complementary studies in mouse have used complex crosses to identify new modifiers such as Cpne8 and provided supporting evidence for previously implicated genes (Rarb and Stmn2).
Subcellular Golgi localization of stathmin family proteins is promoted by a specific set of DHHC palmitoyl transferases.
Chauvin et al., Paris, France. In Mol Biol Cell, 2011
palmitoylation of stathmins 2 and 3 likely occurs at the Golgi and is crucial for their specific subcellular localization and trafficking
Calmyrin1 binds to SCG10 protein (stathmin2) to modulate neurite outgrowth.
Wojda et al., Warsaw, Poland. In Biochim Biophys Acta, 2011
CaMy1 via SCG10 couples Ca(2+) signals with the dynamics of microtubules during neuronal outgrowth in the developing brain.
IKAP/Elp1 involvement in cytoskeleton regulation and implication for familial dysautonomia.
Razin et al., Jerusalem, Israel. In Hum Mol Genet, 2011
SCG10 is upregulated in the IKAP/Elp1-deficient familial dysautonomia cerebrum lending support to the concept that SCG10 elevation can alter the microtubule organization and dynamics
Phosphorylation of SCG10/stathmin-2 determines multipolar stage exit and neuronal migration rate.
Coffey et al., Turku, Finland. In Nat Neurosci, 2011
These findings indicate that the phosphorylation of SCG10 by JNK1 is a fundamental mechanism that governs the transition from the multipolar stage and the rate of neuronal cell movement during cortical development.
Mutations in SCG10 are not involved in Hirschsprung disease.
Hofstra et al., Groningen, Netherlands. In Plos One, 2009
SCG10 is not directly implicated in Hirschsprung diseased evelopment
Genetic risk factors for variant Creutzfeldt-Jakob disease: a genome-wide association study.
Collinge et al., London, United Kingdom. In Lancet Neurol, 2009
and resistance to kuru (p=2.5 x 10(-4)), in a region upstream of STMN2 (the gene that encodes SCG10).
Uses for JNK: the many and varied substrates of the c-Jun N-terminal kinases.
Kobe et al., Australia. In Microbiol Mol Biol Rev, 2006
Many nonnuclear substrates have also been characterized, and these are involved in protein degradation (e.g., the E3 ligase Itch), signal transduction (e.g., adaptor and scaffold proteins and protein kinases), apoptotic cell death (e.g., mitochondrial Bcl2 family members), and cell movement (e.g., paxillin, DCX, microtubule-associated proteins, the stathmin family member SCG10, and the intermediate filament protein keratin 8).
[Molecular mechanisms for the development and aging of the primate central nervous system].
Hayashi, Inuyama, Japan. In Nihon Shinkei Seishin Yakurigaku Zasshi, 2004
Among these signal molecules, we have focused on somatostatin (SRIF), neurotrophins (BDNF, NT-4/5 and NT-3) and their receptors (Trk), growth associated proteins such as GAP-43 and SCG-10 during the development and aging of primate CNS.
Role of the microtubule destabilizing proteins SCG10 and stathmin in neuronal growth.
Cadas et al., Lausanne, Switzerland. In J Neurobiol, 2004
The related proteins SCG10 and stathmin are highly expressed in the developing nervous system.
Neuronal target genes of the neuron-restrictive silencer factor in neurospheres derived from fetuses with Down's syndrome: a gene expression study.
Emson et al., Cambridge, United Kingdom. In Lancet, 2002
FINDINGS: Results of differential display PCR analysis showed that SCG10--a neuron--specific growth-associated protein regulated by the neuron-restrictive silencer factor REST-was almost undetectable in the Down's syndrome sample.
Stathmin and its phosphoprotein family: general properties, biochemical and functional interaction with tubulin.
Sobel et al., Paris, France. In Cell Struct Funct, 1999
Stathmin is also the generic element of a protein family including the neural proteins SCG10, SCLIP and RB3/RB3'/RB3".
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