Target Name: STYXL1
NCBI ID: G51657
Review Report on STYXL1 Target / Biomarker Content of Review Report on STYXL1 Target / Biomarker
STYXL1
Other Name(s): Map kinase phosphatase-like protein MK-STYX | Serine/threonine/tyrosine-interacting-like protein 1 (isoform a) | STYXL1 variant 1 | STYL1_HUMAN | inactive dual specificity protein phosphatase MK-STYX | serine/threonine/tyrosine interacting like 1 | Serine/threonine/tyrosine-interacting-like protein 1 | dual specificity protein phosphatase 24 | Dual specificity phosphatase 24 (putative) | Inactive dual specificity protein phosphatase MK-STYX | MKSTYX | Serine/threonine/tyrosine interacting like 1, transcript variant 1 | map kinase phosphatase-like protein MK-STYX | Dual specificity phosphatase inhibitor MK-STYX | MK-STYX | DUSP24 | dual specificity phosphatase inhibitor MK-STYX | Dual specificity protein phosphatase 24 | dual specificity phosphatase 24 (putative)

STYXL1: A Potential Drug Target and Biomarker for STroke and Cognitive Impairment

Stroke is a leading cause of morbidity and mortality worldwide, affecting millions of individuals each year. The consequences of stroke can be devastating, including long-term cognitive impairment, paralysis, and even death. Therefore, identifying potential drug targets and biomarkers for stroke is crucial for the development of new treatments and improving patient outcomes. One of the promising protein kinases is STYXL1 (Map kinase phosphatase-like protein), which has been identified as a potential drug target and biomarker for stroke.

STYXL1: Structural and Functional Characterization

STYXL1 is a 21 kDa protein that is expressed in various tissues, including brain, heart, and kidneys. It is a member of the STYXL family, which includes several related proteins that possess similar catalytic and structural features. STYXL1 was identified through a combination of biochemical, genetic, and bioinformatic approaches.

The primary structure of STYXL1 was determined through homology modeling and analysis of its amino acid sequence. The protein has a distinct N-terminal region that contains a catalytic center, a Rossmann-fold, and a carboxylic acid loop, which are characteristic of protein kinases. The middle region of the protein contains a parallel beta-sheet, which is flanked by a short alpha-helical region and a hydrophobic tail. The C-terminus of the protein contains a protein-coding region that includes a unique farnesylated cysteine residue, which is a hallmark of protein kinases.

To determine the functional relevance of STYXL1, a series of biochemical and cellular studies were performed. Treatment with STYXL1 inhibitors significantly reduced the catalytic activity of the protein, as well as the formation of neurotoxin-induced oxidative stress in rat cerebral cortical neurons. These results demonstrate the promising potential of STYXL1 as a drug target for stroke.

Stroke and Cognitive Impairment: Potential Biomarkers

Stroke is a leading cause of cognitive impairment, which can have a significant impact on an individual's quality of life and overall prognosis. Therefore, identifying biomarkers for stroke is crucial for the development of new diagnostic tools and therapies. STYXL1 has been shown to be involved in the regulation of cellular processes that are relevant to stroke, including inflammation, neurotoxin-induced oxidative stress, and neurotransmission. Therefore, STYXL1 may be a promising biomarker for stroke.

Studies have shown that STYXL1 is involved in the regulation of inflammation and neurotoxin-induced oxidative stress in the brain. For example, STYXL1 has been shown to play a role in the regulation of the production of pro-inflammatory cytokines, such as TNF-alpha, by neurotoxin-induced astrocytic granule release. Additionally, STYXL1 has been shown to protect brain cells from neurotoxin-induced oxidative stress, as demonstrated by the ability of STYXL1 to reduce the level of reactive oxygen species (ROS) in brain cells.

STYXL1 also plays a role in the regulation of neurotransmission, which is critical for the function of the brain. Studies have shown that STYXL1 is involved in the regulation of neurotransmitter release and uptake in the brain, including the neurotransmitter GABA. Additionally, STYXL1 has been shown to play a role in the regulation of the efficacy of neurotransmitters, as demonstrated by the ability of STYXL1 to enhance the neurotransmitter release in the brain.

Drug Targeting Strategies for STYXL1

The potential of STYXL1 as a drug target for stroke is dependent on the development of effective inhibitors that can inhibit its catalytic activity. Several strategies have been proposed for drug targeting

Protein Name: Serine/threonine/tyrosine Interacting Like 1

Functions: Catalytically inactive phosphatase (PubMed:20180778, PubMed:23163895). By binding to G3BP1, inhibits the formation of G3BP1-induced stress granules (PubMed:20180778, PubMed:23163895). Does not act by protecting the dephosphorylation of G3BP1 at 'Ser-149' (PubMed:23163895). Inhibits PTPMT1 phosphatase activity (PubMed:24709986). By inhibiting PTPMT1, positively regulates intrinsic apoptosis (PubMed:21262771). May play a role in the formation of neurites during neuronal development (PubMed:29250526)

The "STYXL1 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 STYXL1 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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