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FIP1 like 1

FIP1L1, RHE, Fip1-like 1
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. [provided by RefSeq, Oct 2008] (from NCBI)
Top mentioned proteins: PDGFRA, RHCE, CAN, HAD, PDGFR
Papers on FIP1L1
Evidence for Decoupled Electron and Proton Transfer in the Electrochemical Oxidation of Ammonia on Pt(100).
Koper et al., In J Phys Chem Lett, Feb 2016
UNASSIGNED: The two traditional mechanisms of the electrochemical ammonia oxidation consider only concerted proton-electron transfer elementary steps and thus they predict that the rate-potential relationship is independent of the pH on the pH-corrected RHE potential scale.
A case of myeloid neoplasm with FIP1L1-PDGFRA rearrangement without marked peripheral blood eosinophilia.
Ouyang et al., Nanjing, China. In Pharmacogenomics, Jan 2016
We report a 29-year-old man with double hip pain and lower limb weakness for 6 months with myeloid neoplasm with FIP1L1-PDGFRA rearrangement without marked peripheral blood eosinophilia.
Matrix Effect of Human Reconstructed Epidermis on the Chemoselectivity of a Skin Sensitizing α-Methylene-γ-Butyrolactone: Consequences for the Development of in Chemico Alternative Methods.
Lepoittevin et al., Strasbourg, France. In Chem Res Toxicol, Dec 2015
Recently, we have shown that using a high-resolution magic angle spinning (HRMAS) nuclear magnetic resonance (NMR) technique it was possible to characterize chemical interactions taking place between a skin sensitizer and nucleophilic amino acids present in a 3-D reconstructed human epidermis (RHE).
[The Hypereosinophilic Syndromes in Childhood].
Kunzmann et al., Bern, Switzerland. In Klin Padiatr, Nov 2015
While for some subgroups of the HESN (among others FIP1L1-PDGFRA fusion gene) the administration of a tyrosine kinase inhibitor is a new and effective therapy option, glucocorticoids still represent the medication of first choice for many not PDGFRA associated variants.
Controlled Growth of Ferrihydrite Branched Nanosheet Arrays and Their Transformation to Hematite Nanosheet Arrays for Photoelectrochemical Water Splitting.
Qi et al., Beijing, China. In Acs Appl Mater Interfaces, Nov 2015
After a simple postgrowth Ti-doping process, the resulting Ti-doped α-Fe2O3 nanosheet arrays showed a good PEC performance for water splitting with a photocurrent density of 1.79 mA/cm(2) at 1.6 V vs RHE under AM 1.5G illumination (100 mW/cm(2)).
The oncogenic FIP1L1-PDGFRα fusion protein displays skewed signaling properties compared to its wild-type PDGFRα counterpart.
Wiesinger et al., Luxembourg. In Jakstat, 2014
Here, we demonstrate that the oncogenic FIP1L1-PDGFRα kinase exhibits a significantly different signaling pattern compared to its PDGFRα wild type counterpart.
Therapy-related acute myeloid leukemia with eosinophilia, basophilia, t(4;14)(q12;q24) and PDGFRA rearrangement: a case report and review of the literature.
Shao et al., Tampa, United States. In Int J Clin Exp Pathol, 2014
FIP1L1 was not associated with the PDGFRA rearrangement.
Refractory myeloid sarcoma with a FIP1L1-PDGFRA rearrangement detected by clinical high throughput somatic sequencing.
Lindeman et al., Boston, United States. In Exp Hematol Oncol, 2014
Our clinical NGS assay detected an unanticipated FIP1L1-PDGFRA rearrangement in his tumor.
[The hematological malignancies related to primary hypereosinophilia and their diagnostics].
Haus et al., Laizhou, China. In Postepy Hig Med Dosw (online), 2013
Therefore, routine cytogenetic diagnostics should be complemented by FISH with break-apart probes for potentially rearranged genes (e.g., CBFB, ETV6) and unique probes for fusion genes (e.g., FIP1L1-PDGFRA), specific for hypereosinophilia-associated diseases.
Myeloid neoplasms associated with eosinophilia and rearrangement of PDGFRA, PDGFRB, and FGFR1: a review.
Gotlib et al., Augusta, United States. In Int J Lab Hematol, 2013
Conventional cytogenetics (karyotyping) will detect the majority of abnormalities involving PDGFRB and FGFR1, but florescence in situ hybridization (FISH)/molecular studies are required to detect factor interacting with PAP (FIP1L1)-PDGFRA as the characteristic 4q12 interstitial deletion is cryptic.
Diagnostic complexities of eosinophilia.
Fedoriw et al., Chapel Hill, United States. In Arch Pathol Lab Med, 2013
Most notably, chromosomal rearrangements, such as FIP1L1-PDGFRA fusions caused by internal deletions in chromosome 4, are now known to be associated with many chronic eosinophilic leukemias.
Cyclin-dependent kinase 7/9 inhibitor SNS-032 abrogates FIP1-like-1 platelet-derived growth factor receptor α and bcr-abl oncogene addiction in malignant hematologic cells.
Pan et al., Guangzhou, China. In Clin Cancer Res, 2012
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.
Limited clinical activity of nilotinib and sorafenib in FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutation.
Reiter et al., In Leukemia, 2012
Treatment with imatinib is associated with an excellent prognosis in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia in first chronic phase
Identification of JAK2 as a mediator of FIP1L1-PDGFRA-induced eosinophil growth and function in CEL.
Duan et al., Changsha, China. In Plos One, 2011
results strongly suggest that JAK2 is activated by Fip1-like1 (FIP1L1)-platelet-derived growth factor receptor alpha (F/P) and is required for F/P stimulation of cellular proliferation and infiltration in chronic eosinophilic leukemia
Telangiectasia macularis eruptiva perstans: more than skin deep.
Krishnaswamy et al., Johnson City, United States. In Dermatol Reports, 2011
Further genetic testing for mutations of c-kit gene or the FIP1L1 gene may help with disease classification and/or therapeutic approaches.
[Genetic mutations and molecularly-targeted drugs in hypereosinophilic syndromes].
Yamada, Japan. In Arerugi, 2011
FIP1L1/PDGFRA fusion gene-positive myeloproliferative disorders with eosinophilia are discussed.
Validation of a new three-color fluorescence in situ hybridization (FISH) method to detect CHIC2 deletion, FIP1L1/PDGFRA fusion and PDGFRA translocations.
Ketterling et al., Rochester, United States. In Leuk Res, 2009
studied a new FISH method to detect CHIC2 deletion, FIP1L1/PDGFRA fusion and PDGFRA translocation in patients with myeloid neoplasms associated with eosinophilia
Treatment of patients with the hypereosinophilic syndrome with mepolizumab.
Mepolizumab HES Study Group et al., Cincinnati, United States. In N Engl J Med, 2008
Patients were negative for the FIP1L1-PDGFRA fusion gene and required prednisone monotherapy, 20 to 60 mg per day, to maintain a stable clinical status and a blood eosinophil count of less than 1000 per microliter.
PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRα-induced myeloproliferative disease.
Gilliland et al., Boston, United States. In Cancer Cell, 2003
FIP1L1-PDGFRalpha causes hypereosinophilic syndrome (HES) and is inhibited by the tyrosine kinase inhibitor imatinib (Gleevec).
A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.
Gilliland et al., Boston, United States. In N Engl J Med, 2003
The hypereosinophilic syndrome may result from a novel fusion tyrosine kinase - FIP1L1-PDGFRalpha - that is a consequence of an interstitial chromosomal deletion.
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