Contact-dependent promotion of cell migration by the OL-protocadherin–Nap1 interaction

Nakao, Shinsuke; Płatek, Anna E.; Hirano, Shinji; Takeichi, Masatoshi

doi:10.1083/jcb.200802069

Cited by 113 publications

(117 citation statements)

References 43 publications

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“…Each cadherin subtype, which shows a unique tissue distribution, might confer some kind of tissue specificity on the structure and functions of AJs, but this concept has not been tested. The roles of nonclassic cadherins in AJ regulation is another interesting issue, as some protocadherins can down-regulate the functions of classic cadherins (Chen and Gumbiner 2006;Nakao et al 2008). There must be a number of unknown interactions between the classic and nonclassic cadherin systems, as both of their components accumulate at cell-cell contacts.…”

Section: Discussionmentioning

confidence: 99%

Adherens Junction: Molecular Architecture and Regulation

Meng¹,

Takeichi²

2009

Cold Spring Harbor Perspectives in Biology

502

449

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Section: Discussionmentioning

confidence: 99%

Adherens Junction: Molecular Architecture and Regulation

Meng¹,

Takeichi²

2009

Cold Spring Harbor Perspectives in Biology

502

449

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“…The signaling mechanisms linking the diverse protocadherins to the actin cytoskeleton in neurons are still being worked out. Recent studies, however, show that the protocadherins PCDH10 and PCDH19 directly recruit the WAVE1 complex (54,55). This interaction is mediated by a WAVE complex-interacting receptor sequence (WIRS) in the intracellular tail (56).…”

Section: Protocadherinsmentioning

confidence: 99%

Actin Out: Regulation of the Synaptic Cytoskeleton

Spence

Soderling

2015

Journal of Biological Chemistry

153

122

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The small size of dendritic spines belies the elaborate role they play in excitatory synaptic transmission and ultimately complex behaviors. The cytoskeletal architecture of the spine is predominately composed of actin filaments. These filaments, which at first glance might appear simple, are also surprisingly complex. They dynamically assemble into different structures and serve as a platform for orchestrating the elaborate responses of the spine during spinogenesis and experience-dependent plasticity. Multiple mutations associated with human neurodevelopmental and psychiatric disorders involve genes that encode regulators of the synaptic cytoskeleton. A major, unresolved question is how the disruption of specific actin filament structures leads to the onset and progression of complex synaptic and behavioral phenotypes. This review will cover established and emerging mechanisms of actin cytoskeletal remodeling and how this influences specific aspects of spine biology that are implicated in disease.Dendritic spines are morphologically diverse, actin-rich protrusions emerging from dendritic shafts that serve as the receiving sites for the majority of excitatory synaptic transmission in the brain. First described over a century ago by Ramón y Cajal, dendritic spines typically consist of a spine head, which can range in size from 0.5 to 2 m in length, and thin spine neck (ϳ0.2 m thick) (Fig. 1). Their essential function is to compartmentalize biochemical and electrical signals in response to synaptic activation (1). Dendritic spines are supported by an underlying cytoskeleton that is almost exclusively composed of actin filaments, which can be up to ϳ200 nm long (2). Remodeling of this densely packed actin governs most, if not all, dendritic spine physiology. This includes spine formation and maintenance, synaptic adhesion, receptor endocytosis and exocytosis, and synaptic plasticity (Fig. 1). Further, the actin cytoskeleton drives dendritic spine turnover and morphological changes that occur in vivo in response to experience (3). Finally, aberrations in dendritic spine morphology and density are linked to a variety of neurological disorders such as schizophrenia (SZ) 2 and intellectual disability (ID) (4). Recent studies link de novo mutations associated with increased risk of complex psychiatric disorders such as SZ to genes encoding regulators of the post-synaptic actin cytoskeleton (5) (see Fig. 3). Together these findings strongly imply that proper maintenance of the spine actin cytoskeleton is critical for spine functionality and neuronal connectivity. This review will focus on the nuts and bolts of actin dynamics in spines as well as recent developments in the modulation of the synaptic cytoskeleton in two crucial dendritic spine processes whose disturbances are linked with synapse pathologies: synaptic adhesion and synaptic plasticity.

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“…The underlying mechanism is hypothesized to be distinct from that of classical cadherins. PCDH10 interacts with Nck-associated protein 1 (Nap1)/WAVE1, and the PCDH10/Nap1/WAVE1 complex affects actin assembly and subsequently regulates cell migration (26). However, how PCDH10/Nap1/WAVE1 complex controls actin assembly remains unknown.…”

Section: Characteristics and Biological Functions Of Pcdh10mentioning

confidence: 99%

Epigenetic silencing of protocadherin 10 in colorectal cancer

et al. 2017

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Abstract. Colorectal cancer (CRC) is one of the most common types of malignant tumor in the world and occurs through a multi-step process resulting from the accumulation of genetic and epigenetic alterations of the genome. Although the molecular mechanisms of the pathogenesis of CRC remain unclear, the inactivation of tumor suppressor genes (TSGs) through promoter methylation serves an important role. Aberrant methylation is a well-defined marker of CRC. At present, the epigenetic silencing of protocadherin 10 (PCDH10) has been identified as an important TSG with key roles in colorectal carcinogenesis, invasion and metastasis as a frequent and early event. Advances in gene methylation detection in tumor tissues and body fluids have led to the development of non-invasive screening methods for CRC. The present study aimed to review the epigenetic alteration of PCDH10 in CRC development, and the potential of PCDH10 to be a non-invasive biomarker for CRC.

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Contact-dependent promotion of cell migration by the OL-protocadherin–Nap1 interaction

Cited by 113 publications

References 43 publications

Adherens Junction: Molecular Architecture and Regulation

Adherens Junction: Molecular Architecture and Regulation

Actin Out: Regulation of the Synaptic Cytoskeleton

Epigenetic silencing of protocadherin 10 in colorectal cancer

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