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The Role of Microtubule-Associated Serine/Threonine (MAST) Kinases in Development and Illness
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Journal of Phylogenetics & Evolutionary Biology

ISSN: 2329-9002

Open Access

Short Communication - (2024) Volume 12, Issue 1

The Role of Microtubule-Associated Serine/Threonine (MAST) Kinases in Development and Illness

Simon David*
*Correspondence: Simon David, Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK, Email:
Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK

Received: 28-Jan-2024, Manuscript No. JPGEB-24-129380; Editor assigned: 31-Jan-2024, Pre QC No. P-129380; Reviewed: 14-Feb-2024, QC No. Q-129380; Revised: 19-Feb-2024, Manuscript No. R-129380; Published: 28-Feb-2024 , DOI: 10.37421/2329-9002.2024.12.297
Citation: David, Simon. “The Role of Microtubule-Associated Serine/Threonine (MAST) Kinases in Development and Illness.” J Phylogenetics Evol Biol 12 (2024): 297.
Copyright: © 2024 David S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Introduction

Microtubule-associated serine/threonine kinases represent a class of enzymes crucial for regulating cellular processes, including cell division, cytoskeletal dynamics, and intracellular signaling. This article provides an in-depth exploration of the role of MAST kinases in both development and illness. We discuss their structural characteristics, physiological functions, and their involvement in various diseases, highlighting their potential as therapeutic targets. MAST kinases, a family of serine/threonine kinases, play pivotal roles in diverse cellular processes by phosphorylating target proteins involved in cytoskeletal organization, cell cycle progression, and signal transduction pathways. They are named for their association with microtubules, dynamic polymers crucial for intracellular transport, cell shape maintenance, and cell division. Over the years, research has illuminated the significance of MAST kinases in both normal development and pathological conditions. This article aims to dissect the multifaceted roles of MAST kinases in cellular physiology and pathology [1].

Description

MAST kinases belong to the AGC protein kinase A/protein kinase G/protein kinase C family of protein kinases, characterized by their conserved catalytic domain and regulatory regions. Structurally, MAST kinases consist of a catalytic domain at the N-terminus, followed by various regulatory domains, including protein-protein interaction domains, microtubule-binding domains, and antiregulatory regions. The presence of these diverse domains allows MAST kinases to integrate signals from multiple pathways and modulate their activity accordingly. Regulation of Microtubule Dynamics: MAST kinases directly interact with microtubules, influencing their stability and dynamics. Through phosphorylation of microtubule-associated proteins MAST kinases regulate microtubule assembly, disassembly, and organization, crucial for processes such as cell migration, intracellular trafficking, and cell division. MAST kinases play essential roles in cell cycle regulation by modulating the activity of key regulators such as cyclins and cyclin-dependent kinases. Phosphorylation of these regulators by MAST kinases orchestrates cell cycle transitions, ensuring proper progression through the phases of the cell cycle. MAST kinases participate in various signaling pathways, including those mediated by growth factors, hormones, and cytokines. By phosphorylating downstream effectors, MAST kinases modulate cellular responses to extracellular stimuli, regulating processes such as cell proliferation, differentiation, and survival [2].

Dysregulation of MAST kinases has been implicated in various aspects of cancer progression, including uncontrolled cell proliferation, metastasis, and drug resistance. Aberrant expression or activity of MAST kinases can disrupt cell cycle regulation, promote cytoskeletal remodeling, and enhance cancer cell survival, contributing to tumor development and progression. MAST kinases have emerged as critical regulators of neuronal morphology, synaptic plasticity, and axonal transport. Dysregulation of MAST kinases has been linked to neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis where aberrant microtubule dynamics and disrupted intracellular signaling pathways contribute to disease pathogenesis [3]. MAST kinases modulate immune cell function and cytokine signaling, influencing immune responses in various pathological conditions. Altered MAST kinase activity has been implicated in autoimmune diseases, inflammatory disorders, and immune evasion strategies adopted by pathogens, highlighting their role in immune homeostasis and disease pathogenesis [4].

Given their involvement in diverse diseases, MAST kinases represent promising therapeutic targets for intervention. Small molecule inhibitors targeting MAST kinases have shown efficacy in preclinical studies, demonstrating their potential for cancer therapy, neuroprotection, and immune modulation. However, further research is needed to elucidate the specific roles of individual MAST kinase isoforms in different diseases and optimize therapeutic strategies targeting these kinases [5].

Conclusion

In conclusion, MAST kinases are versatile regulators of cellular physiology, exerting profound effects on development, homeostasis, and disease pathogenesis. Their involvement in diverse cellular processes, coupled with their dysregulation in various diseases, underscores the importance of understanding the intricate signaling networks orchestrated by MAST kinases. Further research into the functional roles of MAST kinases and the development of targeted therapeutics hold promise for advancing our understanding of disease mechanisms and improving clinical outcomes for patients with MAST kinase-associated disorders.

Acknowledgement

Not applicable.

Conflict of Interest

There is no conflict of interest by author.

References

  1. Ortmann, Robert A., Tammy Cheng, Roberta Visconti and David M. Frucht, et al. "Janus kinases and signal transducers and activators of transcription: Their roles in cytokine signaling, development and immunoregulation." Arthritis Res Ther 2 (1999): 1-17.
  2. Google Scholar, Crossref, Indexed at

  3. Muneer, Ather. "Wnt and GSK3 signaling pathways in bipolar disorder: Clinical and therapeutic implications." Clin Psychopharmacol Neurosci 15 (2017): 100.
  4. Google Scholar, Indexed at

  5. Abruzzese, Elisabetta, Malgorzata Monika Trawinska, Alessio Pio Perrotti and Paolo De Fabritiis. "Tyrosine kinase inhibitors and pregnancy." Mediterr J Hematol 6 (2014).
  6. Google Scholar, Crossref, Indexed at

  7. Margolis, Russell L. and Christopher A. Ross. "Neuronal signaling pathways: Genetic insights into the pathophysiology of major mental illness." neuropsychopharmacolog 35 (2010): 350.
  8. Google Scholar, Crossref, Indexed at

  9. Sanachai, Kamonpan, Panupong Mahalapbutr, Lueacha Tabtimmai and Supaphorn Seetaha, et al. "In silico and in vitro study of janus kinases inhibitors from naphthoquinones." mol 28 (2023): 597.
  10. Google Scholar, Crossref, Indexed at

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