期刊
TRENDS IN MOLECULAR MEDICINE
卷 17, 期 4, 页码 178-187出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2010.11.005
关键词
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The cell adhesion molecule L1 (L1CAM) was originally identified as a neural adhesion molecule essential for neurite outgrowth and axon guidance. Many studies have now shown that L1CAM is overexpressed in human carcinomas and associated with poor prognosis. So far, L1CAM-mediated cellular signaling has been largely attributed to an association with growth factor receptors, referred to as L1CAM-'assisted' signaling. New data demonstrate that L1CAM can signal via two additional mechanisms: 'forward' signaling via regulated intra-membrane proteolysis and 'reverse' signaling via the activation of the transcription factor nuclear factor (NF)-kappa B. Taken together, these findings lead to a new understanding of L1CAM downstream signaling that is fundamental for the development of anti-L1CAM antibody-mediated therapeutics in human tumor cells.
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