GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
Cacao
| GO:0014047 | glutamate secretion | PMID:22588999 | IMP: Inferred from Mutant Phenotype | P | ||||
| This annotation made on page: By: Thejalsrikumar (group Team CFP) on 2013-03-28 21:23:56 CDT. | ||||||||
You must be logged in to challenge this annotation.
| Entry Type | Challenging User,Group | Time/Date | Challenge Reason | Points/Assessment |
|---|---|---|---|---|
| Challenge | Messanyn, Team The Knockouts | 2013-04-16 14:28:59 CDT | GO term should be: GO:0051823 "Any process that modulates the frequency, rate or extent of synapse structural plasticity. Synapse structural plasticity is a type of cytoskeletal remodeling; this remodeling is induced by stimuli that can lead to long term potentiation and it can be activity-dependent or -independent. Examples of cytoskeletal changes include the formation of new spines and increase in spine size; this can be accompanied by the insertion of greater numbers of glutamate (or other neurotransmitter) receptors into the post-synaptic membrane. " | 0 |
| Challenge | Fkmasuda, Team The Z-team | 2013-04-07 16:56:24 CDT | GO ID should be GO:0023061 and term name: signal release | 0 |
| Challenge | Athena99, Team BTHO PubMed! | 2013-04-03 23:24:41 CDT | GO ID should be GO:0014049 and term name: positive regulation of glutamate secretion. | 0 |
| Challenge | Athena99, Team BTHO PubMed! | 2013-04-02 03:36:14 CDT | The GO ID should be: GO:0014048, with the term name: regulation of glutamate secretion. | 0 |
| Public Assessment | JimHu | 2013-04-28 22:57:37 CDT | It is not clear whether this paper can provide a useful annotation of the wt function of torsin. First, the mutation is dominant so it is not possible to determine whether it is increasing or decreasing the normal function. "In the knock-in model of DYT1 dystonia studied here, the presence of one wild-type and one mutated allele produce a condition paralleling that in patients with the autosomal-dominant DYT1 dystonia (heterozygous for ΔE-torsinA)". Second, the mechanism of the mutation may not reflect either loss or overexpression of the normal function:"According to one hypothesis, the presence of the ΔE-torsinA mutation leads to mislocalization of snapin and other synaptic proteins to sites outside presynaptic nerve terminals, thus causing synaptic abnormalities. However, it is likely that the process is not straightforward (Granata et al.,2009)." | Unacceptable ✗ Go term |
| Public Assessment | DanielRenfro | 2013-04-16 14:28:59 CDT | This annotation has been flagged because it has been edited since last assessment | Flagged |
| Private Assessment | Suzialeksander | 2013-04-07 21:19:01 CDT | You need to be an instructor to view these notes. | Requires Changes ✗ Go term |
| Public Assessment | DanielRenfro | 2013-04-07 16:56:24 CDT | This annotation has been flagged because it has been edited since last assessment | Flagged |
| Private Assessment | Suzialeksander | 2013-04-04 11:18:07 CDT | You need to be an instructor to view these notes. | Requires Changes ✗ Go term |
| Public Assessment | DanielRenfro | 2013-04-03 23:24:41 CDT | This annotation has been flagged because it has been edited since last assessment | Flagged |
| Public Assessment | DanielRenfro | 2013-04-02 03:36:14 CDT | This annotation has been flagged because it has been edited since last assessment | Flagged |
| Private Assessment | Suzialeksander | 2013-03-29 16:48:56 CDT | You need to be an instructor to view these notes. | Requires Changes ✔ Protein ✔ Publication ✔ Qualifier ✗ Go term ✔ Evidence ✔ With/From ✔ Notes ✔ Unique/Original |
