Figure 3.

G3BP participates in some signaling pathways. (A) The Wnt/β-catenin pathway. Axin, and adenomatous polyposis coli (APC) activate glycogen synthase kinase‐3 beta (GSK-3β). This causes the degradation of β-catenin, which is mediated by proteasomes. Wnt3a activates this pathway. Ctnnb1 mRNA in the Dishevelled3 (Dvl3) complex has the ability to resist the degradation of β-catenin and can also stimulate the rapid accumulation of β-catenin in cells. This causes the translocation of β-catenin to the nucleus and stimulates the activation of genes. (B) IL-6 pathway. IL-6 binds to IL-6R and glycoprotein 130 (gp130) on the membrane, dimerizes gp130, and initiates intracellular signals. First, Janus kinase (JAK) is activated, and then STAT3 is phosphorylated to form a homodimer, which is transferred to the nucleus to induce the expression of target genes. IL-6 can also activate the Src, MAPK cascade and PI3K signaling pathway; (C) MAPK/ERK pathway. Growth factors bind to specific receptors on the cell membrane to form dimers. Ras dissociates from GDP and binds to GTP. Ras is first activated, and it further activates the serine/threonine protein kinase (Raf-1), which phosphorylates it, thereby activating MEK; (D) PI3K/Akt mTOR pathway. When growth factor binds to receptors, it can change the protein structure of Akt and further activate the downstream target molecule, mTOR. The tumor suppressor protein PTEN can dephosphorylate Akt and reduce its activation. It can also prevent downstream signal transduction, which is regulated by Akt. It is also a negative regulator of PI3K. (E) P53 signal. P53 is a tumor suppressor gene that can respond to various cell signals such as DNA damage, oncogene expression, nutrient deprivation, and ribosome dysfunction. P53 regulates the genome integrity, cell cycle arrest, and cell apoptosis; (F) NF-κB pathway. When the upstream signal factor binds to the receptor on the cell membrane surface, the receptor conformation changes, and the signal is transmitted to IKK. IκBα is phosphorylated under the action of IKK-α/β, and the phosphorylated IκBα is then ubiquitinated and degraded by the proteasome to release p50/p65. Subsequently, the p50/p65 dimer exposes the nuclear localization sequence (NLS), rapidly enters the nucleus from the cytoplasm, and combines with specific sequences on the nuclear DNA to promote the transcription of related genes; (G) cGAS-STING pathway. cGAS is an important cytoplasmic sensor for DNA and the cGAS-STING pathway is very important for the defense against viral infections. cGAS recognizes exogenous DNA and catalyzes the synthesis of cGAMP. Then, cGAMP binds to and activates STING, recruits TBK1, and phosphorylates IRF3 and activates it to induce the production of interferons.