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Recent News and Articles on the Keywords: protein may + missing protein + autism  Related to the article below (Last Update: 7/1/2008)

Mammalian Clock Protein Responds Directly To Light
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This suggests that cryptochromes may have non-visual functions, and may also affect protein levels and behavior. Hoang et al. ...

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The molecular accelerator is normally kept under control by a tumor-suppressor protein, PTEN, which acts like a brake to curb excess cell growth that could ...
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Homocysteine is a pro-oxidant derived from incomplete protein metabolism. However, it is only one of many problems. More detrimental to heart health is ...
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SEX4, Starch And Phosphorylation: Molecular Mechanisms Of Starch ...
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The SEX4 phosphatase is related to laforin, a protein involved in animal glycogen metabolism. When laforin is missing, insoluble starch-like polyglucosans ...
A to Z of the Olympics
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Human growth hormone Artificial version of a protein that stimulates cell production; increases muscle mass and aids recovery. Injected or taken in capsule ...
Shaping a new lifestyle
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A box of protein bars was missing just one bar. "I thought those would be good for us, but I don't really like them," Julie Erck told Perdomo. ...
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Source: Google News

… in the gene encoding protein kinase c-beta (PRKCB1) on chromosome 16 are associated with autism -
A Philippi, E Roschmann, F Tores, P Lindenbaum, A … - Molecular Psychiatry, 2005 - nature.com
... test with unphased haplotypes (EM algorithm) and missing data. ... genes, the otoancorin
(OTOA) and the protein kinase C ... This may to some extent explain the higher ...

… in the ribosomal protein gene RPL10 suggest a novel modulating disease mechanism for autism -
SM Klauck, B Felder, A Kolb-Kokocinski, C Schuster … - Molecular Psychiatry, 2006 - nature.com
... Alignment of RPL10e/RPL16 protein sequences. ... RPL10[H213Q] found in autism patients
may be functional ... by supplying basic translation functions missing in these ...

… a Common Mechanism of Endoplasmic Reticulum Retention for the {alpha}, beta-Hydrolase Fold Protein … -
A De Jaco, D Comoletti, Z Kovarik, G Gaietta, Z … - Journal of Biological Chemistry, 2006 - ASBMB
... was truncated at residue 529 thereby missing residues 530 ... This heterogeneity of
molecular forms may reflect accumulation of ... species of the mutant protein and/or ...

Mutation analysis of the methyl-CpG-binding protein 2 gene (MECP2) in Rett patients with preserved … -
Y Yamashita, I Kondo, T Fukuda, R Morishima, A … - Brain and Development, 2001 - Elsevier
... One possibility of phenotypic variability may be associated ... The putative protein
has a normal methyl-binding domain (MBD), but is missing a transcriptional ...

The Fragile X mental retardation protein -
B Bardoni, A Schenck, JL Mandel - Brain Research Bulletin, 2001 - Elsevier
... are more evident in late childhood and after puberty, but may be missing in young ...
syndrome thus implicates the analysis of the function of the FMRP protein. ...

… lyase from Pyrobaculum aerophilum reveals an intracellular protein with three disulfide bonds -
EA Toth, C Worby, JE Dixon, ER Goedken, S Marqusee … - Journal of Molecular Biology, 2000 - Elsevier
... disulfide bonds in ASL contribute to protein stability in ... mobility of residues
353?378, may be critical ... a structural alignment, the region missing from the P ...

… of human CADPS and CADPS2, new members of the Ca2+-dependent activator for secretion protein family -
FA Cisternas, JB Vincent, SW Scherer, PN Ray - Genomics, 2003 - Elsevier
... It is possible that mutations in CADPS2 may lead to ... within any known functional domains
of the protein, and thus ... homology to mouse Cadps and was missing the 5 ...

Fragile X syndrome and Autism: Genetics of both Conditions -
WT Brown - autismhellas.gr
... clue about the nature of brain malfunction in autism. ... The specific function of the
missing FMR protein is ... known to be an RNA binding protein, may regulate the ...
-

[CITATION] Methyl-CpG-binding protein (MECP2) polymorphisms and vulnerability to autism
CS Loat, S Curran, CM Lewis, B Abrahams, J Duvall, … - Genes, Brain and Behavior, 2008 - Blackwell Synergy

Autism and Autoimmunity
RS Root-Bernstein - Science News, 1986 - JSTOR
... to the au- toimmune response to myelin basic protein. ... immune system, and that autoim-
munity may be a ... Hospital, Brentwood Los Angeles, Calif Copies Missing? ...

Source: Google Scholar

MIT: Missing protein may be key to autism

CAMBRIDGE, Mass.--A missing brain protein may be one of the culprits behind autism and other brain disorders, researchers at MIT's Picower Institute for Learning and Memory report in the Dec. 6 issue of Neuron.

The protein helps synapses develop. Synapses--through which neurons communicate with one other-underlie our ability to learn and remember. Now Li-Huei Tsai, Picower Professor of Neuroscience at MIT, has uncovered an enzyme that is key to that protein's activity.

Synapses are complex structures consisting of ion channels, receptors and intricate protein complexes that all work together to send and receive signals. Improperly formed synapses could lead to mental retardation, and mutations in genes encoding certain synaptic proteins are associated with autism.

Tsai studies a kinase (kinases are enzymes that change proteins) called Cdk5. While Cdk5's best-known role is to help new neurons form and migrate to their correct positions during brain development, “emerging evidence supports an important role for Cdk5 at the synapse,” she said.

To gain a better understanding of how Cdk5 promotes synapse formation, Tsai's lab looked into how Cdk5 interacts with synapse-inducing proteins-in particular, a protein called CASK. CASK--a key scaffolding protein-is one of the first proteins on the scene of a developing synapse.

Scaffolding proteins such as CASK are like site managers, supporting protein-to-protein interactions to ensure that the resulting architecture is sound. Mutations in the genes responsible for Cdk5 and CASK have been found in mental retardation patients.

“We found that Cdk5 is critical for recruiting CASK to do its job for developing synapses,” Tsai said. “Without Cdk5, CASK was not in the right place at the right time, and failed to interact with essential presynaptic components. This, in turn, led to problems with calcium influx.” The flow of calcium in and out of neurons affects processes central to nervous system development and plasticity--its ability to change in response to experience.

Gene mutations and/or deletions in synaptic cell surface proteins and molecules called neurexins and neuroligins have been associated with autism. The problem with CASK recruitment investigated by the Tsai laboratory creates the same result as these genetic changes.

The Picower study also provides the first molecular explanation of how Cdk5, which also may go awry in neurodegenerative diseases such as Alzheimer's, promotes synapse development.

"There are still a lot of unknowns," said Tsai, who is also a Howard Hughes Medical Institute investigator. "Causes for psychiatric disorders are still very unclear, but accumulating evidence strongly suggests that alterations in the synaptogenesis program can lead to these serious diseases.”

###

In addition to Tsai and Picower researcher Benjamin A. Samuels, co-authors are associated with Harvard Medical School; Johns Hopkins University School of Medicine; McLean Hospital in Belmont, Mass.; and Academia Sinica in Taiwan.

This work is supported by the National Institute of Neurological Disorders and Stroke (NINDS).
 
 
 
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