Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mouse neuroblastoma (MNB) cells infected with ERA virus were specifically lysed in the presence of rabbit complement by antisera produced in mice to challenge virus standard (CVS), ERA, Flury HEP or street virus (SV) strains of rabies. MNB or EL-4 cells persistently infected with ERA, MNB cells infected with CVS, and BHK-21/S13 cells infected with ERA or Flury HEP also were suitable targets. CER cells infected with either ERA, CVS or Flury HEP, BHK-21/S13 cells infected with CVS and MNB cells infected with Flury HEP were not suitable targets. Two unusual findings indicated that 1. some cells which were greater than 80 percent positive for rabies viral membrane antigen(s) were poorly lysed, and 2. some cells that expressed cytoplasmic antigen lacked detectable membrane antigens.
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PMID:Influence of cell type and virus upon lysis of rabies virus-infected cells by antibody and complement. 733 91

Activation of the EGFR pathway is one of the mechanisms inducing acquired resistance to anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKI) such as crizotinib and alectinib. Ceritinib is a highly selective ALK inhibitor and shows promising efficacy in non-small cell lung cancers (NSCLC) harboring the ALK gene rearrangement. However, the precise mechanism underlying acquired resistance to ceritinib is not well-defined. This study set out to clarify the mechanism in ALK-translocated lung cancer and to find the preclinical rationale overcoming EGFR pathway-induced acquired resistance to ALK-TKIs. To this end, ceritinib-resistant cells (H3122-CER) were established from the H3122 NSCLC cell line harboring the ALK gene rearrangement via long-term exposure to ceritinib. H3122-CER cells acquired resistance to ceritinib through EGFR bypass pathway activation. Furthermore, H3122 cells that became resistant to ceritinib or alectinib through EGFR pathway activation showed cross-resistance to other ALK-TKIs. Ceritinib and afatinib combination treatment partially restored the sensitivity to ceritinib.
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PMID:Overcoming EGFR Bypass Signal-Induced Acquired Resistance to ALK Tyrosine Kinase Inhibitors in ALK-Translocated Lung Cancer. 2770 87