PRKCD: A Protein Regulator of Cell Signaling, Inflammation and Stress Response

Target Name: PRKCD

NCBI ID: G5580

PRKCD

PRKCD: A Protein Regulator of Cell Signaling, Inflammation and Stress Response

PRKCD (Proteasome-Resetting Kallikrein-Dependent Compound) is a protein that is expressed in various tissues throughout the body. It is a key regulator of the proteasome, a complex that helps to break down and remove proteins that are no longer needed. PRKCD has been shown to be involved in a wide range of physiological processes, including cell signaling, inflammation, and stress response. As a result, PRKCD has generated a lot of interest as a potential drug target or biomarker.

The proteasome is a complex that consists of a set of proteins that work together to break down and remove proteins that are no longer needed. This complex is essential for maintaining cellular homeostasis and for the regulation of many cellular processes. One of the key proteins that is involved in the proteasome is Kallikrein, which is a type of enzyme that is known for its role in the regulation of blood clotting.

PRKCD is a protein that is expressed in various tissues throughout the body, including the brain, heart, and kidneys. It is a key regulator of the proteasome, and it has been shown to play a role in the regulation of many cellular processes. For example, PRKCD has been shown to be involved in the regulation of cell signaling, inflammation, and stress response.

One of the key functions of PRKCD is its role in the regulation of cell signaling. PRKCD has been shown to play a role in the regulation of many different signaling pathways, including the TGF-β pathway, the PI3K/Akt pathway, and the NF-kappa-B pathway. These pathways are important for the regulation of many different cellular processes, including cell growth, differentiation, and inflammation.

PRKCD is also involved in the regulation of inflammation. It has been shown to play a role in the regulation of the production of pro-inflammatory cytokines, such as TNF-伪 and IL-1尾. These cytokines are important for the regulation of many different cellular processes, including inflammation, pain, and stress.

In addition to its role in cell signaling and inflammation, PRKCD is also involved in the regulation of stress response. It has been shown to play a role in the regulation of cellular stress responses, including the regulation of DNA damage and the expression of genes involved in stress response.

As a result of its involvement in these different cellular processes, PRKCD has generated a lot of interest as a potential drug target or biomarker. Many researchers are interested in the regulation of PRKCD as a potential therapeutic approach for a wide range of diseases, including cancer, neurodegenerative diseases, and autoimmune diseases.

In conclusion, PRKCD is a protein that is expressed in various tissues throughout the body and is involved in the regulation of many different cellular processes. It has generated a lot of interest as a potential drug target or biomarker due to its role in the regulation of cell signaling, inflammation, and stress response. Further research is needed to fully understand the function of PRKCD and its potential as a therapeutic approach for a wide range of diseases.

Protein Name: Protein Kinase C Delta

Functions: Calcium-independent, phospholipid- and diacylglycerol (DAG)-dependent serine/threonine-protein kinase that plays contrasting roles in cell death and cell survival by functioning as a pro-apoptotic protein during DNA damage-induced apoptosis, but acting as an anti-apoptotic protein during cytokine receptor-initiated cell death, is involved in tumor suppression as well as survival of several cancers, is required for oxygen radical production by NADPH oxidase and acts as positive or negative regulator in platelet functional responses (PubMed:21810427, PubMed:21406692). Negatively regulates B cell proliferation and also has an important function in self-antigen induced B cell tolerance induction (By similarity). Upon DNA damage, activates the promoter of the death-promoting transcription factor BCLAF1/Btf to trigger BCLAF1-mediated p53/TP53 gene transcription and apoptosis (PubMed:21810427, PubMed:21406692). In response to oxidative stress, interact with and activate CHUK/IKKA in the nucleus, causing the phosphorylation of p53/TP53 (PubMed:21810427, PubMed:21406692). In the case of ER stress or DNA damage-induced apoptosis, can form a complex with the tyrosine-protein kinase ABL1 which trigger apoptosis independently of p53/TP53 (PubMed:21810427, PubMed:21406692). In cytosol can trigger apoptosis by activating MAPK11 or MAPK14, inhibiting AKT1 and decreasing the level of X-linked inhibitor of apoptosis protein (XIAP), whereas in nucleus induces apoptosis via the activation of MAPK8 or MAPK9. Upon ionizing radiation treatment, is required for the activation of the apoptosis regulators BAX and BAK, which trigger the mitochondrial cell death pathway. Can phosphorylate MCL1 and target it for degradation which is sufficient to trigger for BAX activation and apoptosis. Is required for the control of cell cycle progression both at G1/S and G2/M phases. Mediates phorbol 12-myristate 13-acetate (PMA)-induced inhibition of cell cycle progression at G1/S phase by up-regulating the CDK inhibitor CDKN1A/p21 and inhibiting the cyclin CCNA2 promoter activity. In response to UV irradiation can phosphorylate CDK1, which is important for the G2/M DNA damage checkpoint activation (By similarity). Can protect glioma cells from the apoptosis induced by TNFSF10/TRAIL, probably by inducing increased phosphorylation and subsequent activation of AKT1 (PubMed:15774464). Is highly expressed in a number of cancer cells and promotes cell survival and resistance against chemotherapeutic drugs by inducing cyclin D1 (CCND1) and hyperphosphorylation of RB1, and via several pro-survival pathways, including NF-kappa-B, AKT1 and MAPK1/3 (ERK1/2). Involved in antifungal immunity by mediating phosphorylation and activation of CARD9 downstream of C-type lectin receptors activation, promoting interaction between CARD9 and BCL10, followed by activation of NF-kappa-B and MAP kinase p38 pathways (By similarity). Can also act as tumor suppressor upon mitogenic stimulation with PMA or TPA. In N-formyl-methionyl-leucyl-phenylalanine (fMLP)-treated cells, is required for NCF1 (p47-phox) phosphorylation and activation of NADPH oxidase activity, and regulates TNF-elicited superoxide anion production in neutrophils, by direct phosphorylation and activation of NCF1 or indirectly through MAPK1/3 (ERK1/2) signaling pathways (PubMed:19801500). May also play a role in the regulation of NADPH oxidase activity in eosinophil after stimulation with IL5, leukotriene B4 or PMA (PubMed:11748588). In collagen-induced platelet aggregation, acts a negative regulator of filopodia formation and actin polymerization by interacting with and negatively regulating VASP phosphorylation (PubMed:16940418). Downstream of PAR1, PAR4 and CD36/GP4 receptors, regulates differentially platelet dense granule secretion; acts as a positive regulator in PAR-mediated granule secretion, whereas it negatively regulates CD36/GP4-mediated granule release (PubMed:19587372). Phosphorylates MUC1 in the C-terminal and regulates the interaction between MUC1 and beta-catenin (PubMed:11877440). The catalytic subunit phosphorylates 14-3-3 proteins (YWHAB, YWHAZ and YWHAH) in a sphingosine-dependent fashion (By similarity). Phosphorylates ELAVL1 in response to angiotensin-2 treatment (PubMed:18285462). Phosphorylates mitochondrial phospholipid scramblase 3 (PLSCR3), resulting in increased cardiolipin expression on the mitochondrial outer membrane which facilitates apoptosis (PubMed:12649167). Phosphorylates SMPD1 which induces SMPD1 secretion (PubMed:17303575)

The "PRKCD 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 PRKCD 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