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. 2017 Feb 28;97(1):23–40. doi: 10.1007/s41745-016-0011-3

Figure 3:

Figure 3:

Representation of cellular functions of inositol pyrophosphates in an eukaryotic cell. 1 IP7 physiologically inhibits AKT signalling by competitively binding to the PH domain of AKT and thus preventing it from binding to PI(3,4,5)P3 (PIP3). IP7 and IP6K2 promote, 2 apoptosis and 3 formation of autophagosomes. 4 PP-IPs regulate the cellular levels of ATP by their action on the glycolysis pathway and mitochondrial membrane potential. 5 IP7 is responsible for maintaining endoplasmic reticulum morphology in yeast cells. 6 IP7-mediated pyrophosphorylation regulates dynein binding to membranes and thereby influences Golgi morphology. 7 PP-IPs positively regulate the synthesis of polyphosphates in yeast vacuoles. 8 In pancreatic β cells, IP7 upregulates insulin secretion by increasing the readily releasable pool of insulin granules docked at the plasma membrane. 9 IP7 inhibits the synaptic exocytotic pathway in neurons. In the nucleus, PP-IPs are responsible for 10 telomere length maintenance in yeast, 11 DNA repair via the homologous recombination (HR) and nucleotide excision repair (NER) pathways, and 12 epigenetic modifications that influence chromatin remodelling to control global transcription. 13 In yeast, IP7 influences ribosome biogenesis by regulating nucleolar rDNA transcription.