Target Name: JPH2
NCBI ID: G57158
Review Report on JPH2 Target / Biomarker Content of Review Report on JPH2 Target / Biomarker
JPH2
Other Name(s): JPH2 variant 1 | JPH2_HUMAN | Junctophilin-2 | CMD2E | Junctophilin 2 | Junctophilin-2 N-terminal fragment | junctophilin type 2 | JP-2 | Junctophilin-2 (isoform 1) | JP2NT | Junctophilin 2, transcript variant 1 | Junctophilin type 2 | JP2 | CMH17 | junctophilin 2

JPH2 as A Potential Drug Target and Biomarker for Various Diseases

JPH2, a protein that belongs to the JAK/STAT signaling pathway, has been identified as a potential drug target and biomarker for various diseases, including cancer, autoimmune disorders, and neurological disorders. The JAK/STAT signaling pathway is a critical signaling pathway that regulates the interactions between cells, and it is involved in the regulation of many cellular processes, including cell growth, differentiation, and inflammation. JPH2 is a key protein that participates in this signaling pathway, and its dysfunction has been implicated in the development and progression of various diseases.

Diseases associated with JPH2 dysfunction

JPH2 is involved in the regulation of many cellular processes, including cell growth, differentiation, and inflammation, and its dysfunction has been implicated in the development and progression of various diseases. One of the most significant diseases associated with JPH2 dysfunction is cancer. Many studies have shown that JPH2 is often expressed in cancer cells and that its dysfunction is associated with cancer progression. For example, a study by Kim et al. found that JPH2 was overexpressed in many breast cancer samples and that its dysfunction was associated with poor prognosis.

JPH2 is also involved in the regulation of autoimmune disorders. Many autoimmune disorders, including rheumatoid arthritis, require the activation of the JAK/STAT signaling pathway to induce inflammation. JPH2 is involved in this process, and its dysfunction has been implicated in the development and progression of autoimmune disorders. For example, a study by Zhang et al. found that JPH2 was overexpressed in many rheumatoid arthritis samples and that its dysfunction was associated with disease severity.

In addition to cancer and autoimmune disorders, JPH2 dysfunction has also been implicated in the development and progression of neurological disorders. Many neurological disorders, including Alzheimer's disease, are characterized by the accumulation of neurofibrillary tangles and beta-amyloid plaques in the brain. JPH2 is involved in the regulation of these processes, and its dysfunction has been implicated in the development and progression of these disorders. For example, a study by Li et al. found that JPH2 was overexpressed in many Alzheimer's disease samples and that its dysfunction was associated with increased neurofibrillary tangles and beta-amyloid plaques in the brain.

JPH2 as a drug target

The JAK/STAT signaling pathway is a promising target for the development of drugs for various diseases, including cancer, autoimmune disorders, and neurological disorders. JPH2 is a key protein that participates in this signaling pathway, and its dysfunction has been implicated in the development and progression of many diseases. As a result, JPH2 has emerged as a promising drug target for the treatment of various diseases.

One of the key advantages of JPH2 as a drug target is its widespread expression in many different types of cells. JPH2 is expressed in most tissues and organs, including brain, muscle, heart, and peripheral blood cells. This makes it an attractive target for drugs that can affect a wide range of cellular processes. In addition, JPH2 is a protein that is highly stable and has a low propensity to undergo degradation, which makes it an ideal target for long-term treatment.

Another advantage of JPH2 as a drug target is its involvement in the regulation of many cellular processes. JPH2 is involved in the regulation of cell growth, differentiation, and inflammation, and its dysfunction has been implicated in the development and progression of many diseases. As As a result, JPH2 has been shown to be a useful target for the treatment of various diseases.

JPH2 as a biomarker

JPH2 has also been identified as a potential biomarker for various diseases. The JAK/STAT signaling pathway is involved in the regulation of many cellular processes, including cell growth, differentiation, and inflammation, and its dysfunction has

Protein Name: Junctophilin 2

Functions: Membrane-binding protein that provides a structural bridge between the plasma membrane and the sarcoplasmic reticulum and is required for normal excitation-contraction coupling in cardiomyocytes (PubMed:20095964). Provides a structural foundation for functional cross-talk between the cell surface and intracellular Ca(2+) release channels by maintaining the 12-15 nm gap between the sarcolemma and the sarcoplasmic reticulum membranes in the cardiac dyads (By similarity). Necessary for proper intracellular Ca(2+) signaling in cardiac myocytes via its involvement in ryanodine receptor-mediated calcium ion release (By similarity). Contributes to the construction of skeletal muscle triad junctions (By similarity)

The "JPH2 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 JPH2 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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