MYLK: A Potential Drug Target for Muscle and Cellular Processes

Target Name: MYLK

NCBI ID: G4638

MYLK

MYLK: A Potential Drug Target for Muscle and Cellular Processes

Myosin Light Chain Kinase (MYLK) is a protein that plays a crucial role in the regulation of muscle growth and maintenance. It is a key enzyme in the myosin light chain (MLC) complex, which is responsible for generating the force necessary for muscle growth and movement.

MYLK is a 21-kDa protein that is expressed in muscle fibers and is responsible for the kinetic properties of the MLC. It functions as a negative regulator of myosin ATPase, which is the protein that powers muscle contraction. When muscle fibers contract, the MLC is broken and the ATPase is activated, leading to the release of calcium ions and the initiation of muscle contraction.MYLK helps to regulate the speed and strength of muscle contractions by controlling the activity of the ATPase.

MYLK has also been shown to play a role in the regulation of muscle mass and bone density. It has been shown to enhance the expression of genes involved in muscle growth and development, and to inhibit the expression of genes involved in muscle loss. This suggests that MYLK may have potential as a drug target for muscle-related diseases, such as muscle dystrophy and myopathies.

In addition to its role in muscle growth and maintenance, MYLK has also been shown to have potential as a biomarker for a variety of diseases. For example, it has been shown to be involved in the development of cancer, and to be a potential therapeutic target for cancer treatment. Additionally, its role in the regulation of inflammation has also been suggested, andMYLK has been shown to play a role in the regulation of immune cell function.

MYLK is also involved in the regulation of the cytoskeleton, which is the structure that gives shape to the cell. It is a key component of the cytoskeleton and helps to maintain the integrity of the cell. This suggests that MYLK may have potential as a drug target for diseases that affect the cytoskeleton, such as fibromyalgia and multiple sclerosis.

In conclusion, MYLK is a protein that plays a crucial role in the regulation of muscle growth and maintenance. Its role as a negative regulator of myosin ATPase and its involvement in the regulation of muscle mass, bone density, and inflammation suggest that it may have potential as a drug target or biomarker for a variety of diseases. Further research is needed to fully understand the role of MYLK in these processes and to develop effective treatments.

Protein Name: Myosin Light Chain Kinase

Functions: Calcium/calmodulin-dependent myosin light chain kinase implicated in smooth muscle contraction via phosphorylation of myosin light chains (MLC). Also regulates actin-myosin interaction through a non-kinase activity. Phosphorylates PTK2B/PYK2 and myosin light-chains. Involved in the inflammatory response (e.g. apoptosis, vascular permeability, leukocyte diapedesis), cell motility and morphology, airway hyperreactivity and other activities relevant to asthma. Required for tonic airway smooth muscle contraction that is necessary for physiological and asthmatic airway resistance. Necessary for gastrointestinal motility. Implicated in the regulation of endothelial as well as vascular permeability, probably via the regulation of cytoskeletal rearrangements. In the nervous system it has been shown to control the growth initiation of astrocytic processes in culture and to participate in transmitter release at synapses formed between cultured sympathetic ganglion cells. Critical participant in signaling sequences that result in fibroblast apoptosis. Plays a role in the regulation of epithelial cell survival. Required for epithelial wound healing, especially during actomyosin ring contraction during purse-string wound closure. Mediates RhoA-dependent membrane blebbing. Triggers TRPC5 channel activity in a calcium-dependent signaling, by inducing its subcellular localization at the plasma membrane. Promotes cell migration (including tumor cells) and tumor metastasis. PTK2B/PYK2 activation by phosphorylation mediates ITGB2 activation and is thus essential to trigger neutrophil transmigration during acute lung injury (ALI). May regulate optic nerve head astrocyte migration. Probably involved in mitotic cytoskeletal regulation. Regulates tight junction probably by modulating ZO-1 exchange in the perijunctional actomyosin ring. Mediates burn-induced microvascular barrier injury; triggers endothelial contraction in the development of microvascular hyperpermeability by phosphorylating MLC. Essential for intestinal barrier dysfunction. Mediates Giardia spp.-mediated reduced epithelial barrier function during giardiasis intestinal infection via reorganization of cytoskeletal F-actin and tight junctional ZO-1. Necessary for hypotonicity-induced Ca(2+) entry and subsequent activation of volume-sensitive organic osmolyte/anion channels (VSOAC) in cervical cancer cells. Responsible for high proliferative ability of breast cancer cells through anti-apoptosis

The "MYLK Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about MYLK comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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