http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2014038223-A1

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assignee http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_82a308524dd92f08d281d392c66fe6f7
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_b7fda957fc47ca407f28adc2893a1040
classificationCPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-5011
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classificationIPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/G01N33-50
filingDate 2012-03-30-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_8df592a8bacf34994e3d154723264cd2
publicationDate 2014-02-06-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-2014038223-A1
titleOfInvention Crk-a novel target for cancer therapy
abstract This disclosure identifies a novel apoptotic compensatory proliferation signaling complex (ASCS) involving ExoT's cellular target, Crk1. This disclosure demonstrates that in cells induced to undergo apoptosis, Crk1 forms globular complexes which associate with plasma membrane in the apoptotic cell and are released from the dying cell to its healthy neighbor, inducing it to proliferate. ExoT prevents the ACSC assembly while inducing apoptosis, indicating that apoptotic program cell death and compensatory proliferation are distinct and can be uncoupled from each other. Without being bound to any particular theory, it is believed that Crk1 functions as a scaffold for the ACSC assembly and that its ADP-ribosylation by ExoT interferes with this process while resulting in anoikis apoptotic cell death.
priorityDate 2011-03-31-04:00^^<http://www.w3.org/2001/XMLSchema#date>
type http://data.epo.org/linked-data/def/patent/Publication

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