PIP5K1C: A Potential Drug Target for Cancer and Diabetes (G23396)

Target Name: PIP5K1C

NCBI ID: G23396

PIP5K1C

PIP5K1C: A Potential Drug Target for Cancer and Diabetes

Phosphatidylinositol-4-phosphate (PIP) is a crucial signaling molecule in various cellular processes, including cell signaling, intracellular signaling, and cell survival. PIP5K1C, a gene encoding a protein involved in the intracellular signaling pathway known as the PI3K/AKT signaling pathway , has been identified as a potential drug target or biomarker for various diseases, including cancer, diabetes, and cardiovascular diseases.

PIP5K1C function

The PI3K/AKT signaling pathway is a highly conserved intracellular signaling pathway that plays a pivotal role in various cellular processes, including cell survival, angiogenesis, and inflammation. The pathway is composed of several key components, including the protein kinase A (PKA), the protein inhibitor尾-catenin, and the protein tyrosine phosphatase kinase (PTP).

PIP5K1C is a key protein kinase. The kinase active site is a conserved kinase active site and participates in the PI3K/AKT signaling pathway.

PIP5K1C gene

The PIP5K1C gene is located on human chromosome 11 and encodes a protein with a length of 1,914 amino acids. The expression product of this gene is localized to the cytoplasm and plays a role within the cell. The expression level of PIP5K1C gene can be affected by many factors, including cell cycle, growth factors, ion concentration and protein kinases.

Biological functions of PIP5K1C

PIP5K1C is a key enzyme in the PI3K/AKT signaling pathway and participates in the intracellular signal transduction process. Studies have shown that PIP5K1C is up-regulated in a variety of tumors, and its expression level is positively correlated with tumor growth and progression. At the same time, the expression level of PIP5K1C is also related to the invasion and metastasis ability of tumors.

Pharmacological significance of PIP5K1C

Since the upregulation of PIP5K1C in tumors is related to the biological behavior of tumors, PIP5K1C is considered a potential tumor therapeutic target. Currently, there are many studies devoted to developing anti-tumor drugs for PIP5K1C. For example, the use of PIP5K1C inhibitors can significantly inhibit tumor growth and progression and improve the survival rate of tumor patients.

Biological significance of PIP5K1C

PIP5K1C is a key protein involved in the PI3K/AKT signaling pathway. Its upregulation is associated with tumor growth and progression and is therefore considered a potential tumor therapeutic target. PIP5K1C inhibitors can significantly inhibit tumor growth and progression and improve the survival rate of tumor patients.

Protein Name: Phosphatidylinositol-4-phosphate 5-kinase Type 1 Gamma

Functions: Catalyzes the phosphorylation of phosphatidylinositol 4-phosphate (PtdIns(4)P/PI4P) to form phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2/PIP2), a lipid second messenger that regulates several cellular processes such as signal transduction, vesicle trafficking, actin cytoskeleton dynamics, cell adhesion, and cell motility (PubMed:12422219, PubMed:22942276). PtdIns(4,5)P2 can directly act as a second messenger or can be utilized as a precursor to generate other second messengers: inositol 1,4,5-trisphosphate (IP3), diacylglycerol (DAG) or phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3/PIP3) (Probable). PIP5K1A-mediated phosphorylation of PtdIns(4)P is the predominant pathway for PtdIns(4,5)P2 synthesis (By similarity). Together with PIP5K1A, is required for phagocytosis, both enzymes regulating different types of actin remodeling at sequential steps (By similarity). Promotes particle attachment by generating the pool of PtdIns(4,5)P2 that induces controlled actin depolymerization to facilitate Fc-gamma-R clustering. Mediates RAC1-dependent reorganization of actin filaments. Required for synaptic vesicle transport (By similarity). Controls the plasma membrane pool of PtdIns(4,5)P2 implicated in synaptic vesicle endocytosis and exocytosis (PubMed:12847086). Plays a role in endocytosis mediated by clathrin and AP-2 (adaptor protein complex 2) (PubMed:12847086). Required for clathrin-coated pits assembly at the synapse (PubMed:17261850). Participates in cell junction assembly (PubMed:17261850). Modulates adherens junctions formation by facilitating CDH1/cadherin trafficking (PubMed:17261850). Required for focal adhesion dynamics. Modulates the targeting of talins (TLN1 and TLN2) to the plasma membrane and their efficient assembly into focal adhesions (PubMed:12422219). Regulates the interaction between talins (TLN1 and TLN2) and beta-integrins (PubMed:12422219). Required for uropodium formation and retraction of the cell rear during directed migration (By similarity). Has a role in growth factor-stimulated directional cell migration and adhesion (By similarity). Required for talin assembly into nascent adhesions forming at the leading edge toward the direction of the growth factor (PubMed:17635937). Negative regulator of T-cell activation and adhesion (By similarity). Negatively regulates integrin alpha-L/beta-2 (LFA-1) polarization and adhesion induced by T-cell receptor (By similarity). Together with PIP5K1A has a role during embryogenesis and together with PIP5K1B may have a role immediately after birth (By similarity)

The "PIP5K1C 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 PIP5K1C 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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