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- B883dd0108bc61f9fd60f0fef7f9b623f NCIT_P378 "NCI" @default.
- B883dd0108bc61f9fd60f0fef7f9b623f type Axiom @default.
- B883dd0108bc61f9fd60f0fef7f9b623f annotatedProperty IAO_0000115 @default.
- B883dd0108bc61f9fd60f0fef7f9b623f annotatedSource NCIT_C185862 @default.
- B883dd0108bc61f9fd60f0fef7f9b623f annotatedTarget "The maleate salt form of flonoltinib, an orally bioavailable dual inhibitor of both Janus-associated kinase 2 (JAK2) and of FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon oral administration, flonoltinib targets, binds to and inhibits the activity of both JAK2 and FLT3. This prevents the activation of the JAK/signal transducer and activator of transcription (STAT) signaling pathway and the activation of STAT3 and STAT5 as well as FLT3-mediated signaling. This may lead to an induction of apoptosis and a decrease in proliferation of tumor cells in which JAK2 and FLT3 are overexpressed. In addition, as JAK2 and FLT3 play a key role in the regulation of the inflammatory response and dendritic cell (DC) proliferation, differentiation and function, inhibition of JAK2- and FLT3-mediated signaling may suppress the generation and differentiation of DCs, and may regulate inflammatory and immune responses. JAK2, often upregulated or mutated in a variety of cancer cells, mediates STAT3 activation and plays a key role in tumor cell proliferation and survival. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias." @default.