Scaffold mediated regulation of MAPK signaling and cytoskeletal dynamics: A perspective

Pullikuth, Ashok; Catling, Andrew D.

doi:10.1016/j.cellsig.2007.04.012

Cited by 138 publications

(113 citation statements)

References 233 publications

(264 reference statements)

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“…Activation of the ERK pathway has been found to function in proliferation, cell death, and cytoskeletal remodeling, by translocating to the nucleus and activating transcript factors (Chambard et al, 2007;Dumesic et al, 2009;Pullikuth and Catling, 2007). Both transient and sustained activations of ERK1/2 phosphorylate downstream Elk and induce c-Fos expression during cell cycle procession (Chambard et al, 2007;Dumesic et al, 2009).…”

Section: Mapk Signaling Erk1/2mentioning

confidence: 99%

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MAPK signaling in inflammation-associated cancer development

2010

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Mitogen-activated protein (MAP) kinases comprise a family of protein-serine/threonine kinases, which are highly conserved in protein structures from unicellular eukaryotic organisms to multicellular organisms, including mammals. These kinases, including ERKs, JNKs and p38s, are regulated by a phosphorelay cascade, with a prototype of three protein kinases that sequentially phosphorylate one another. MAPKs transduce extracellular signals into a variety of cellular processes, such as cell proliferation, survival, death, and differentiation. Consistent with their essential cellular functions, MAPKs have been shown to play critical roles in embryonic development, adult tissue homeostasis and various pathologies. In this review, we discuss recent findings that reveal the profound impact of these pathways on chronic inflammation and, particularly, inflammation-associated cancer development.

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Section: Mapk Signaling Erk1/2mentioning

confidence: 99%

“…ERK scaffolding proteins also appear important in transmitting signals to adhesion turnover sites. For more details, please refer to the review by Pullikuth and Catling (2007).…”

Section: Mapk Signaling Erk1/2mentioning

confidence: 99%

MAPK signaling in inflammation-associated cancer development

2010

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“…The use of protein scaffolds to link regulators within defined signalling pathways or at particular locations in the cell is a frequently inferred mechanism to explain the role of protein complex formation [114,115]. However, the term scaffold has not been used in a consistent manner and can imply distinct mechanistic scenarios.…”

Section: Scaffolds As Potential Flexible Linkagesmentioning

confidence: 99%

Yeast and fungal morphogenesis from an evolutionary perspective

Wedlich‐Söldner

2008

Seminars in Cell & Developmental Biology

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Cellular morphogenesis is a complex process and molecular studies in the last few decades have amassed a large amount of information that is difficult to grasp in any completeness. Fungal systems, in particular the budding and fission yeasts, have been important players in unravelling the basic structural and regulatory elements involved in a wide array of cellular processes. In this article, we address the design principles underlying the various processes of yeast and fungal morphogenesis. We attempt to explain the apparent molecular complexity from the perspective of the evolutionary theory of "facilitated variation". Following a summary of some of the most studied morphogenetic phenomena, we discuss, using recent examples, the underlying core processes and their associated "weak" regulatory linkages that bring about variation in morphogenetic phenotypes.

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“…Furthermore, BDNF-and GDNF-induced neuronal differentiations require cAMP up-regulation (30), whereas NGF promotes neurite growth in a cAMP-independent manner (31). It has also been established that these neurotrophins use the mitogen-activated protein kinase (MAPK) pathway to promote neurite growth (32), and this pathway is known to regulate scaffold and cytoskeletal dynamics in response to neurotrophic factors (33). However, the molecular mechanisms responsible for actin assembly downstream of MAPK have not been established in the context of neurotrophin-induced neuritogenesis.…”

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confidence: 99%

Axonal Neuropathy-associated TRPV4 Regulates Neurotrophic Factor-derived Axonal Growth

Jang

Jung

Kim

et al. 2012

Journal of Biological Chemistry

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Background:Because genetic linkage studies identified mutations in TRPV4 in patients with peripheral neuropathies, the function of TRPV4 in peripheral neurons is questioned. Results: TRPV4 was found to promote neurotrophic factor-driven neuritogenesis. Conclusion: TRPV4 mediates neurotrophic factor-driven neuritogenesis in peripheral neurons. Significance: This explains molecular mechanisms underlying neuritogenesis and maintenance of peripheral nerves.

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Scaffold mediated regulation of MAPK signaling and cytoskeletal dynamics: A perspective

Cited by 138 publications

References 233 publications

MAPK signaling in inflammation-associated cancer development

MAPK signaling in inflammation-associated cancer development

Yeast and fungal morphogenesis from an evolutionary perspective

Axonal Neuropathy-associated TRPV4 Regulates Neurotrophic Factor-derived Axonal Growth

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