Target Name: PKP2
NCBI ID: G5318
Review Report on PKP2 Target / Biomarker Content of Review Report on PKP2 Target / Biomarker
PKP2
Other Name(s): plakophilin 2 | Plakophilin 2, transcript variant 2a | Plakophilin-2 (isoform 2a) | Plakophilin 2, transcript variant 2b | PKP2_HUMAN | Plakophilin-2 | ARVD9 | Plakophilin-2 (isoform 2b) | Plakophilin 2 | PKP2 variant 2a | PKP2 variant 2b

PKP2: A Potential Drug Target and Biomarker

Plakophilin (PKP) is a protein that is expressed in various cell types, including neurons, muscle cells, and blood vessels. It is involved in the regulation of cell signaling pathways and has been implicated in a number of diseases, including cardiovascular disease, diabetes, and neurodegenerative disorders. In recent years, researchers have been interested in developing drugs that target PKP2 to treat various diseases. In this article, we will explore the potential of PKP2 as a drug target and biomarker.

The Protein Kinase C (PKC) Signaling Pathway

PKC is a protein that is involved in cell signaling pathways and is a key regulator of many cellular processes. It is composed of two main isoforms, PKC伪 and PKC尾, which are involved in different cellular functions. PKC伪 is predominantly expressed in neurons and is involved in the regulation of neurotransmitter signaling, while PKC尾 is predominantly expressed in muscle cells and is involved in the regulation of muscle contraction.

PKP2 is a 21-kDa protein that is predominantly expressed in neural cells, including neurons and glial cells. It is a negative regulator of PKC and has been shown to inhibit the activity of PKC伪. This means that when PKP2 is expressed in a cell, it can prevent PKC伪 from activating, which can lead to the inhibition of cellular signaling pathways.

The Potential Benefits of Targeting PKP2

Targeting PKP2 has the potential to treat a variety of diseases. One of the main targets of PKP2 is neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. These disorders are characterized by the progressive loss of brain cells and can cause a range of symptoms, including cognitive decline, tremors, and difficulty with movement.

In addition to neurodegenerative disorders, PKP2 has also been shown to be involved in a number of other diseases, including cardiovascular disease and diabetes. For example, PKP2 has been shown to be involved in the regulation of Angiotensin II, a hormone that contributes to the development of hypertension and cardiovascular disease. It has also been shown to be involved in the regulation of glucose metabolism and may play a role in the development of type 2 diabetes.

The Structure and Function of PKP2

The structure of PKP2 is highly conserved and is similar to that of other proteins that are involved in the regulation of PKC signaling pathways. It consists of a 196 amino acid residue and has a calculated molecular mass of 21 kDa. PKP2 has a single transmembrane domain and a number of putative intracellular loops.

PKP2 is involved in the regulation of PKC signaling by inhibiting the activity of PKC伪. This can be done through a variety of mechanisms, including the formation of a covalent complex with PKC伪, the inhibition of PKC伪 activity by direct interactions with its regulatory domain, or the inhibition of PKC伪 by modifying its activity.

PKP2 Interacts with Other Proteins

PKP2 has been shown to interact with a number of other proteins, including several transcription factors, such as NF-kappa-B, AP-1, and STAT3. It has also been shown to interact with a variety of cytoskeletal proteins, including microtubules and actin. These interactions may be involved in the regulation of PKP2 activity and may contribute to its effects on cellular signaling pathways.

Drugs that Target PKP2

Several drugs that target PKP2 have been developed and are in clinical trials for the treatment of various diseases. These drugs include inhibitors of PKP2 itself, such as PKP2 inhibitors, as well as drugs that target PKP2-interactive proteins.

In

Protein Name: Plakophilin 2

Functions: Regulates focal adhesion turnover resulting in changes in focal adhesion size, cell adhesion and cell spreading, potentially via transcriptional modulation of beta-integrins (PubMed:23884246). Required to maintain gingival epithelial barrier function (PubMed:34368962). Required for cardiac sodium current propagation and electrical synchrony in cardiac myocytes (By similarity). Required for the formation of desmosome cell junctions in cardiomyocytes, thereby required for the correct formation of the heart, specifically trabeculation and formation of the atria walls (By similarity). Loss of desmosome cell junctions leads to mis-localization of DSP and DSG2 resulting in disruption of cell-cell adhesion and disordered intermediate filaments (By similarity). Modulates profibrotic gene expression in cardiomyocytes via regulation of DSP expression and subsequent activation of downstream TGFB1 and MAPK14/p38 MAPK signaling (By similarity). May play a role in junctional plaques (PubMed:22781308). Involved in the inhibition of viral infection by influenza A viruses (IAV) (PubMed:28169297). Acts as a host restriction factor for IAV viral propagation, potentially via disrupting the interaction of IAV polymerase complex proteins (PubMed:28169297)

The "PKP2 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 PKP2 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

More Common Targets

PKP3 | PKP4 | PKP4-AS1 | PLA1A | PLA2G10 | PLA2G12A | PLA2G12AP1 | PLA2G12B | PLA2G15 | PLA2G1B | PLA2G2A | PLA2G2C | PLA2G2D | PLA2G2E | PLA2G2F | PLA2G3 | PLA2G4A | PLA2G4B | PLA2G4C | PLA2G4D | PLA2G4E | PLA2G4F | PLA2G5 | PLA2G6 | PLA2G7 | PLA2R1 | PLAA | PLAAT1 | PLAAT2 | PLAAT3 | PLAAT4 | PLAAT5 | PLAC1 | PLAC4 | PLAC8 | PLAC8L1 | PLAC9 | PLAC9P1 | PLAG1 | PLAGL1 | PLAGL2 | Plasma Membrane Calcium ATPase | PLAT | Platelet Glycoprotein Ib Complex | Platelet-activating factor acetylhydrolase isoform 1B complex | Platelet-Derived Growth Factor (PDGF) | Platelet-Derived Growth Factor Receptor | PLAU | PLAUR | PLB1 | PLBD1 | PLBD1-AS1 | PLBD2 | PLCB1 | PLCB2 | PLCB3 | PLCB4 | PLCD1 | PLCD3 | PLCD4 | PLCE1 | PLCE1-AS2 | PLCG1 | PLCG1-AS1 | PLCG2 | PLCH1 | PLCH2 | PLCL1 | PLCL2 | PLCXD1 | PLCXD2 | PLCXD3 | PLCZ1 | PLD1 | PLD2 | PLD3 | PLD4 | PLD5 | PLD6 | PLEC | PLEK | PLEK2 | PLEKHA1 | PLEKHA2 | PLEKHA3 | PLEKHA4 | PLEKHA5 | PLEKHA6 | PLEKHA7 | PLEKHA8 | PLEKHA8P1 | PLEKHB1 | PLEKHB2 | PLEKHD1 | PLEKHF1 | PLEKHF2 | PLEKHG1 | PLEKHG2 | PLEKHG3 | PLEKHG4