BCR-FGFR1-associated PI3K phosphorylates PIP2 to PIP3.

Stable Identifier
R-HSA-1839107
Type
Reaction [transition]
Species
Homo sapiens
Compartment
ReviewStatus
5/5
Locations in the PathwayBrowser
General
SVG |   | PPTX  | SBGN
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout
Once recruited to the activated BCR-FGFR1 fusion PI3K phosphorylates PIP2 to PIP3, leading to activation of AKT signaling (Roumiantsev, 2004; Demiroglu, 2001).
Literature References
PubMed ID Title Journal Year
11739186 The t(8;22) in chronic myeloid leukemia fuses BCR to FGFR1: transforming activity and specific inhibition of FGFR1 fusion proteins

Doody, ML, Demiroglu, A, Carnicero, F, Brody, JP, Melo, JV, Koduru, P, Cross, NC, Heath, C, Hawson, G, Taylor, K, Steer, EJ, Goldman, JM, Reiter, A, Rodwell, R, Bentley, M, Allen, SL

Blood 2001
15050920 Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocations

Krause, DS, Dimitri, CA, Asiedu, F, Van Etten, RA, Cross, NC, Roumiantsev, S, Neumann, CA

Cancer Cell 2004
Participants
Participates
Catalyst Activity

phosphatidylinositol-4,5-bisphosphate 3-kinase activity of pY177-BCR-pY-FGFR1 mutant:GRB2:p-GAB1:PI3K [cytosol]

Normal reaction
Functional status

Gain of function of pY177-BCR-pY-FGFR1 mutant:GRB2:p-GAB1:PI3K [cytosol]

Status
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
chronic myeloid leukemia DOID:8552 CML, chronic myelogenous leukemia, no ICD-O subtype (morphologic abnormality), chronic myeloid leukemia, disease (disorder), chronic myeloid leukemia without mention of remission, CML - chronic Myelogenous Leukemia, chronic myeloid leukemia in remission (disorder), Myeloid Leukemia, chronic, CML in Remission, chronic myeloid leukemia in remission, chronic myeloid leukaemia, chronic myeloid leukemia NOS (disorder)
Cross References
Rhea
Authored
Reviewed
Created
Cite Us!