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FIP1L1 encodes a subunit of the CPSF (cleavage and polyadenylation specificity factor) complex that polyadenylates the 3' end of mRNA precursors. Additionally we are shipping FIP1 Like 1 (S. Cerevisiae) Antibodies (34) and FIP1 Like 1 (S. Cerevisiae) Proteins (3) and many more products for this protein.
F604S exchange in FIP1L1-PDGFRA (show PDGFRA ELISA Kits) enhances FIP1L1-PDGFRA (show PDGFRA ELISA Kits) protein stability via SHP-2 (show PTPN11 ELISA Kits) and SRC (show SRC ELISA Kits) and is associated with kinase inhibitor resistance in hypereosinophilic syndrome and chronic eosinophilic leukemia.
FIP1L1 differentially contributes to the pathogenesis of distinct types of leukemia.
FP fusion gene favors secondary KIT mutations in MCs (show SMCP ELISA Kits) via growth and proliferation signals or that a yet unknown mechanism causes genomic instability with independent evolution of FP and KIT D816V
Oncostatin M (show OSM ELISA Kits) is a FIP1L1/PDGFRA (show PDGFRA ELISA Kits)-dependent mediator of cytokine production in chronic eosinophilic leukemia.
description of polycythemia vera (show IGF2BP3 ELISA Kits) concurrent with FIP1L1-PDGFRA (show PDGFRA ELISA Kits)-positive myeloproliferative neoplasm with eosinophilia [case report]
Data show that the cyclin-dependent kinase 7/9 inhibitor (CDK7/9 inhibitor) potently inhibits FIP1L1-PDGFRalpha-positive Bcr-Abl-positive chronic myeloid leukemia (CML) cells.
results strongly suggest that JAK2 (show JAK2 ELISA Kits) is activated by Fip1 (show RRAGA ELISA Kits)-like1 (FIP1L1)-platelet-derived growth factor receptor alpha (show PDGFRA ELISA Kits) (F/P) and is required for F/P stimulation of cellular proliferation and infiltration in chronic eosinophilic leukemia
Treatment with imatinib is associated with an excellent prognosis in FIP1L1-PDGFRA (show PDGFRA ELISA Kits)-positive chronic eosinophilic leukemia in first chronic phase
FIP1L1/PDGFRA (show PDGFRA ELISA Kits) fusion gene-positive myeloproliferative disorders with eosinophilia are discussed.
The hypereosinophilic syndrome may result from a novel fusion tyrosine kinase (show TXK ELISA Kits) - FIP1L1-PDGFRalpha - that is a consequence of an interstitial chromosomal deletion.
FIP1L1-PDGFRalpha activation requires disruption of the juxtamembrane domain of PDGFRalpha and is FIP1L1-independent
This gene encodes a subunit of the CPSF (cleavage and polyadenylation specificity factor) complex that polyadenylates the 3' end of mRNA precursors. This gene, the homolog of yeast Fip1 (factor interacting with PAP), binds to U-rich sequences of pre-mRNA and stimulates poly(A) polymerase activity. Its N-terminus contains a PAP-binding site and its C-terminus an RNA-binding domain. An interstitial chromosomal deletion on 4q12 creates an in-frame fusion of human genes FIP1L1 and PDGFRA (platelet-derived growth factor receptor, alpha). The FIP1L1-PDGFRA fusion gene encodes a constitutively activated tyrosine kinase that joins the first 233 amino acids of FIP1L1 to the last 523 amino acids of PDGFRA. This gene fusion and chromosomal deletion is the cause of some forms of idiopathic hypereosinophilic syndrome (HES). This syndrome, recently reclassified as chronic eosinophilic leukemia (CEL), is responsive to treatment with tyrosine kinase inhibitors. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
FIP1 like 1
, FIP1-like 1 protein
, pre-mRNA 3'-end-processing factor FIP1
, FIP1L1 cleavage and polyadenylation specific factor subunit
, factor interacting with PAP
, rearranged in hypereosinophilia