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Adaptors for disorders of the brain? The cancer signaling proteins NEDD9, CASS4, and PTK2B in Alzheimer's disease
Journal article   Open access

Adaptors for disorders of the brain? The cancer signaling proteins NEDD9, CASS4, and PTK2B in Alzheimer's disease

Tim N. Beck, Emmanuelle Nicolas, Meghan C. Kopp and Erica A. Golemis
Oncoscience, v 1(7), pp 486-503
23 Jul 2014
DOI: https://doi.org/10.18632/oncoscience.64
PMID: 25594051
url
https://doi.org/10.18632/oncoscience.64View
Published, Version of Record (VoR) Open

Abstract

Alzheimer's disease Amyloid APP Brain CAK-β Cancer CAS CASS4 HEF1 HEPL NEDD9 Neurodegenerative PSEN1 PSEN2 PTK2B PYK2 RAFTK Tau
No treatment strategies effectively limit the progression of Alzheimer's disease (AD), a common and debilitating neurodegenerative disorder. The absence of viable treatment options reflects the fact that the pathophysiology and genotypic causes of the disease are not well understood. The advent of genome-wide association studies (GWAS) has made it possible to broadly investigate genotypic alterations driving phenotypic occurrences. Recent studies have associated single nucleotide polymorphisms (SNPs) in two paralogous scaffolding proteins, NEDD9 and CASS4, and the kinase PTK2B, with susceptibility to late-onset AD (LOAD). Intriguingly, NEDD9, CASS4, and PTK2B have been much studied as interacting partners regulating oncogenesis and metastasis, and all three are known to be active in the brain during development and in cancer. However, to date, the majority of studies of these proteins have emphasized their roles in the directly cancer relevant processes of migration and survival signaling. We here discuss evidence for roles of NEDD9, CASS4 and PTK2B in additional processes, including hypoxia, vascular changes, inflammation, microtubule stabilization and calcium signaling, as potentially relevant to the pathogenesis of LOAD. Reciprocally, these functions can better inform our understanding of the action of NEDD9, CASS4 and PTK2B in cancer.

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