Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation based on Enzyme Commission mapping
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
RasC is required for optimal activation of adenylyl cyclase and Akt/PKB during aggregation.
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RasC is required for aggregation and acts downstream of the cAMP receptor to activate both PI3K/Akt-PKB and adenylyl cyclase.
"RasC appears to be a central regulatory molecule acting downstream of serpentine receptor stimulation by cAMP that is required for two distinct effector pathways: the activation of Akt/PKB through PI3K and the activation of adenylyl cyclase."
Chemoattractant-induced Ras activation during Dictyostelium aggregation.
Loss of the Dictyostelium RasC protein alters vegetative cell size, motility and endocytosis.
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rasC-null vegetative cells have reduced random motility, reduced polarity, altered F-actin, larger size, and normal cytokinesis.
"reduced random motility, were less polarized and had altered F-actin"
The effect of the disruption of a gene encoding a PI4 kinase on the developmental defect exhibited by Dictyostelium rasC(-) cells.
Delineation of the roles played by RasG and RasC in cAMP-dependent signal transduction during the early development of Dictyostelium discoideum.
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RasG is more important for chemotaxis while RasC is more important for adenylyl cyclase (cAMP relay) activation, with partial functional overlap.
"signal transduction through RasC is more important in ACA activation"
Cyclic AMP signalling in Dictyostelium: G-proteins activate separate Ras pathways using specific RasGEFs.
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RasGEFA (Aimless) specifically activates RasC, and RasC is responsible for adenylyl cyclase activation whereas RasG regulates chemotaxis.
"RasGEFA catalysed the removal of GDP from RasC but not from other Ras subfamily proteins, confirming that RasGEFA is specific for RasC"
Rap1 activation in response to cAMP occurs downstream of ras activation during Dictyostelium aggregation.
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RasC/RasG are the presumptive GTPases required for cAMP-induced guanylyl cyclase activation, and Rap1 acts downstream of the Ras proteins.
"guanylyl cyclase activation is also abolished in the"
Nanovesicles released by Dictyostelium cells: a potential carrier for drug delivery.
A Ras signaling complex controls the RasC-TORC2 pathway and directed cell migration.
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A Sca1/RasGEF/PP2A complex is enriched at the leading edge and controls RasC activation and the downstream TORC2-PKB pathway; active Ras is enriched at the leading edge.
"active Ras is enriched at the leading edge of chemotaxing cells"
Ras-mediated activation of the TORC2-PKB pathway is critical for chemotaxis.
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RasC is required for and directly binds/activates TORC2, setting the temporal dynamics of PKBR1/PKBA phosphorylation independently of PIP3.
"RasC is required for TORC2-mediated activation of PKB"
Ras proteins have multiple functions in vegetative cells of Dictyostelium.
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RasC can partially substitute for RasG in folate chemotaxis, but not for RasG's growth/cytokinesis or random-motility functions.
"to folate, RasC is capable of partially substituting for RasG"
Delineating the core regulatory elements crucial for directed cell migration by examining folic-acid-mediated responses.
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RasC activates the TORC2 complex, which triggers PKBA and PKBR1, in a pathway parallel to RasG/PI3K during folate and cAMP responses.
"Ras C activates the TORC2 complex, which in turn triggers PKBA and a second PKB homolog, PKBR1"
Dictyostelium lipid droplets host novel proteins.
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High-throughput identification of the Dictyostelium lipid-droplet proteome.
"Among the novel protein components are LdpA, a protein specific to Dictyostelium"
Regulation of a LATS-homolog by Ras GTPases is important for the control of cell division.
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NdrC (LATS2 homolog) binds RasG/RasB (and less strongly RasC/Rap1); cell division is controlled by RasG/RasB, not by RasC.
"NdrC was the only protein that bound RasC in the yeast two-hybrid screen"
A large-scale screen reveals genes that mediate electrotaxis in Dictyostelium discoideum.
PP2A/B56 and GSK3/Ras suppress PKB activity during Dictyostelium chemotaxis.
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The PP2A regulatory subunit B56 preferentially binds GDP-bound RasC and RasD (not RasG) and contributes to suppression of PKB activity.
"GDP forms of RasC and RasD, but not with RasG in vitro"
The novel RacE-binding protein GflB sharpens Ras activity at the leading edge of migrating cells.
The small GTPases Ras and Rap1 bind to and control TORC2 activity.
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Active RasC binds the catalytic domain of TOR, while Rap1 binds RIP3/SIN1; both control TORC2 activity, with RasC playing the major role.
"we found that TOR kinase itself specifically co-purifies with RasCGppNHp"
Extracellular polyphosphate signals through Ras and Akt to prime Dictyostelium discoideum cells for development.
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Polyphosphate signals through RasC and Akt to inhibit the proteasome and induce CsA expression, priming cells for development.
"mediated by Akt proteins and RasC in Dictyostelium"
GPCR-controlled membrane recruitment of negative regulator C2GAP1 locally inhibits Ras signaling for adaptation and long-range chemotaxis.
An endogenous chemorepellent directs cell movement by inhibiting pseudopods at one side of cells.
Phosphorylated Rho-GDP directly activates mTORC2 kinase towards AKT through dimerization with Ras-GTP to regulate cell migration.
Hetero-oligomerization of Rho and Ras GTPases Connects GPCR Activation to mTORC2-AKT Signaling.
An Autocrine Negative Feedback Loop Inhibits Dictyostelium discoideum Proliferation through Pathways Including IP3/Ca(2).
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Under low-nutrient conditions, loss of RasC blocks polyphosphate-induced proliferation inhibition.
"the loss of GrlD or RasC blocked the sensitivity of cells to polyphosphate"
OpenScientist focused rasC GO:0044351 hypothesis report
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Report recommendation was critically incorporated; the disputed molecular/process claim remains UNDECIDED because the report does not resolve the decisive primary evidence.
"there is no such deletion-uptake dataset in evidence either way"