METTL23: Regulating Microtubules and Cell Signaling (G124512)

Target Name: METTL23

NCBI ID: G124512

METTL23

METTL23: Regulating Microtubules and Cell Signaling

METTL23, also known as METTL23 variant 2, is a protein that is expressed in various tissues throughout the body, including the brain, heart, and kidneys. It is a key regulator of microtubules, which are the structural elements that give cells their shape and help them move and communicate.

METTL23 is a member of the METTL family of proteins, which are known for their role in regulating microtubules. The METTL family consists of six proteins that share a conserved catalytic core and a unique N-terminus. The METTL23 protein is a variant of the METTL23 gene, which is located on chromosome 6p21.

METTL23 is expressed in a wide range of tissues, including the brain, heart, and kidneys. It is highly expressed in the brain, where it is the most abundant protein in the microtubules. METTL23 is also expressed in the heart and kidneys, where it is involved in regulating the structure and function of the heart muscle and the vasculature.

One of the unique features of METTL23 is its ability to regulate the formation of microtubules. Microtubules are dynamic structures that give cells their shape and help them move and communicate. METTL23 is involved in the regulation of microtubule formation by promoting the formation of long microtubules and preventing the formation of short ones. This helps to ensure that cells maintain their proper shape and function.

METTL23 is also involved in the regulation of microtubule dynamics. Microtubules are constantly in motion, and their dynamics are regulated by a variety of factors, including the concentration of motor proteins. METTL23 is involved in the regulation of the concentration of these proteins, which helps to ensure that the microtubules maintain their proper stability.

METTL23 is also involved in the regulation of cell signaling pathways. It is a negative regulator of the protein kinase CKL, which is involved in cell signaling pathways. This means that when CKL is activated, METTL23 is inhibited, and when it is deactivated, METTL23 is activated. This helps to ensure that cells maintain proper signaling pathways and that signaling pathways are not activated when they should not be.

METTL23 is also involved in the regulation of cell adhesion. It is a negative regulator of the protein Smad, which is involved in cell adhesion. This means that when Smad is activated, METTL23 is inhibited, and when it is deactivated, METTL23 is activated. This helps to ensure that cells maintain proper cell-cell adhesion and that they do not detach from each other.

METTL23 is also involved in the regulation of cell migration. It is a negative regulator of the protein vimentin, which is involved in cell migration. This means that when vimentin is activated, METTL23 is inhibited, and when it is deactivated, METTL23 is activated. This helps to ensure that cells move and migrate properly and that they do not detach from each other.

METTL23 is also involved in the regulation of the cytoskeleton. It is a negative regulator of the protein Myosin, which is involved in cytoskeletal structure. This means that when Myosin is activated, METTL23 is inhibited, and when it is deactivated, METTL23 is activated. This helps to ensure that cells maintain proper cytoskeletal structure and that they do not

Protein Name: Methyltransferase Like 23

Functions: Histone methyltransferase that dimethylates histone H3 at 'Arg-17', forming asymmetric dimethylarginine (H3R17me2a), leading to activate transcription via chromatin remodeling (By similarity). Maternal factor involved in epigenetic chromatin reprogramming of the paternal genome in the zygote: mediates H3R17me2a, promoting histone H3.3 incorporation in the male pronucleus, leading to TET3 recruitment and subsequent DNA demethylation (By similarity)

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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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