Pathways

Phytate biosynthesis is a pathway that occurs in the cytosol by which myo-inositol becomes D-myo-inositol (1,3,4)-trisphosphate becomes phytate, the principal storage form of phosphorus in many plant tissues . First, myo-inositol-1,3,4-trisphosphate 5/6-kinase uses ATP to catalyze the conversion of D-myo-inositol (1,3,4)-trisphosphate into either D-myo-inositol (1,3,4,6)-tetrakisphosphate or D-myo-inositol (1,3,4,5)-tetrakisphosphate. It requires magnesium ion as a cofactor. Second, inositol polyphosphate multiple-kinase uses ATP to catalyze the conversion of either D-myo-inositol (1,3,4,6)-tetrakisphosphate or D-myo-inositol (1,3,4,5)-tetrakisphosphate into D-myo-inositol 1,3,4,5,6-pentakisphosphate. Third, polyphosphate 2-kinase uses ATP to catalyze the conversion of D-myo-inositol 1,3,4,5,6-pentakisphosphate into phytate. It requires zinc ion as a cofactor.

Activation of different types of RTKs leads to the activation of PI3K. This causes the conversion of PIP2 to PIP3 at the plasma membrane. Inactive AKT translocate from the cytoplasm to the plasma membrane where PIP3 binds AKT, leading to activation of AKT by phosphorylation by PDK1 and mTOR. The arrows and the bars represent activation and inhibition of the following proteins, respectively.

about pi3K also known as phosphotidylinositol 3 Kinase involved in AKT signalling and is the main activator of PIP2.

Pibrentasvir is a direct acting antiviral agent and Hepatitis C virus (HCV) nonstructural protein 5A inhibitor that targets the the viral RNA replication and viron assembly. In combination with Glecaprevir. Hepatitis C virus lipoviroparticles enter target hepatocytes via receptor-mediated endocytosis. The lipoviroparticles attach to LDL-R and SR-B1, and then the virus binds to CD81 and subsequently claudin-1 and occludin, which mediate the late steps of viral entry. The virus is internalized by clathrin-dependent endocytosis. RNA is released from the mature Hepatitis C virion and translated at the rough endoplasmic reticulum into a single Genome polyprotein. The genome polyprotein is cleaved by host and viral proteases into 10 viral proteins. The nucleocapsid protein core and the two envelope proteins E1 and E2 form the N terminus of the polyprotein and are the structural components of HCV virions. The precursor also gives rise to the viroporin p7 and six non-structural (NS) proteins. Pibrentasvir is an inhibitor of the Hepatitis C Virus (HCV) Nonstructural protein 5A, which is required for viral RNA replication and assembly of HCV virions. The exact mechanism of this protein is unknown. NS5A inhibitors compete with RNA for binding at this site. Viral RNA replication complexes localize to lipid raft-containing, detergent-resistant membranes created by the viral protein NS4B.ding site is exposed. For full viral replication and maturation, replication complexes need to be in close proximity to lipid droplets, which requires the protein nonstructural protein 5A. Without the lipid droplet due to inhibition of nonstructural protein 5A, full viral RNA replication is unable to occur. Envelope glycoproteins are acquired through budding into the endoplasmic reticulum lumen. The immature, non-infective virions are released via the cellular golgi apparatus.