EC Number   |
General Information |
Reference |
|---|
   2.7.1.153 | evolution |
class 1 phosphoinositide 3-kinases are heterodimers consisting of an 85 kDa regulatory/adapter subunit (p85) coupled to a 110 kDa catalytic subunit (p110) with both subunits possessing several isoforms. The class I enzymes are further subdivided into two subclasses: class Ia and class Ib. The class 1a phosphoinositol 3-kinases (p110alpha, p110beta and p110delta) signal downstream of tyrosine kinases, while the single class Ib phosphoinositol 3-kinase (p110gamma) operates downstream of heterotrimeric GPCRs (G-protein-coupled receptors) |
737882 |
| 2.7.1.153 | evolution |
class I PI3K genes control the activity of PI3K/AKT signaling and are often genetically altered in glioblastoma. Class II PI3K genes are implicated in regulating angiogenesis and cilium function. Class III PI3K genes are primarily involved in the regulation of autophagy. Compared to other class IA PI3K isoforms, PIK3CB is the only PI3K catalytic subunit that showed a strong association with recurrence rate, risk, and prognosis |
761163 |
| 2.7.1.153 | malfunction |
a combination of INPP4B overexpression and rucaparib blocks the PI3K/AKT signal pathway |
751184 |
| 2.7.1.153 | malfunction |
a patient with a somatic gain of function PIK3CA-mutation (a pathogenic heterozygous missense mutation in PIK3CA) shows extensive multisystem overgrowth, clinical diversity of the PIK3CA-related overgrowth spectrum (PROS), phenotype, overview. The patient has overlapping features of congenital lipomatous overgrowth vascular malformations epidermal nevi and skeletal abnormalities (CLOVES) syndrome and megalencephaly-capillary malformation polymicrogyria (MCAP) syndrome |
762096 |
| 2.7.1.153 | malfunction |
aberrant activation of the phosphatidylinositol 3-kinase pathway is involved in a wide range of cancers. Mutations in subunit isoform p110alpha are involved in development of bladder cancer, and are also common in the benign skin lesions seborrheic keratosis and epidermal nevi |
707974 |
| 2.7.1.153 | malfunction |
aberrant PI3K signaling has been found to play an important role in multiple aspects of tumorgenesis including uncontrolled proliferation, resistance to apoptosis, angiogenesis and metastatic capability. The PI3Kbeta isoform is implicated as necessary for transformation induced by the loss or inactivation of the PTEN tumor suppressor both in vitro and in vivo |
709907 |
| 2.7.1.153 | malfunction |
binding of thyroid receptor to p85alpha activates PI3K/AKT signaling promoting thyroid carcinogenesis by increasing cell proliferation and tumor metastasis |
710574 |
| 2.7.1.153 | malfunction |
chronic blockade of phosphatidylinositol 3-kinase in the nucleus tractus solitarii is prohypertensive in the spontaneously hypertensive rat |
708686 |
| 2.7.1.153 | malfunction |
constitutively activated phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin, mTOR, signaling is a common feature of T-cell acute lymphoblastic leukemia, where it strongly influences growth and survival |
707979 |
| 2.7.1.153 | malfunction |
deregulated signaling through phosphatidylinositol 3'-kinase pathway is common in many types of malignancies, including mantle cell lymphoma. PI3K catalytic subunit alpha gene amplification contributes to the pathogenesis of mantle cell lymphoma. Inhibition of PIK3CA induces apoptosis in mantle cell lymphoma cell lines |
708158 |
