FBXW7


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FBXW7

A gene on chromosome 4q31.3 that encodes a so-called F-box protein, which contains a 40 amino acid protein-interacting motif (the F box). F-box proteins form a complex with SKP1 and cullin, resulting in phosphorylation-dependent ubiquitination and ubiquitin-mediated degradation of targeted proteins. F-box proteins are divided into three classes based on the presence of:
(1) WD-40 repeats—as is the case with this F-box protein (Fbws class),
(2) leucine-rich repeats (Fbls class); or
(3) the presence or absence of other protein-protein interacting domains (Fbxs class).
The FBXW7 protein product binds directly to cyclin E, targeting it for ubiquitin-mediated degradation.

Molecular pathology
FBXW7 mutations are found in ovarian and breast cancer cell lines, implicating FBXW7’s potential role in carcinogenesis.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.
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Laboratory Performance for Detection of Somatic Variants Genomic Nucleotide Protein Description Gene Transcript Change Change (hg19) AKT1 NM_005163.2 c.49G>A p.E17K chr14:105,246, 551 C>T ALK NM_004304.4 c.38240A p.R1275Q chr2:2 9,432, 6640T BRAF NM_004333.4 c.1799T>A P.V600E chr7:140,453, 136A>T ECFR NM_005228.3 c.21550A P.G719S chr7:55,241, 707G>A FBXW7 NM_033632.3 c.13940A P.R465H chr4:153,249, 3840T IDH1 NM_005896.2 c.3950A P.R132H chr2:209,113, 1120T KIT NM_000222.2 c.1961T>C P.V654A chr4:55,594, 258T>C KRAS NM_004985.3 c.38G>A p.G13D chr12:25,398, 2810T NRAS NM_002524.4 c.182A>G p.Q61R chrl:115,256, 529T>C PIK3CA NM_006218.2 c.3140A>G p.H1047R chr3:178,952, 085A>G Total No.
The lentivirus covered coding region FBXW7 cDNA sequence, and the negative control lentivirus was purchased from Genechem (GeneChem Inc., Shanghai, China).
Two LCNECs demonstrated investigational targets including RET substitution (16 p.M918T c.2753T>C) and FBXW7 mutation (p.Q275X, c.823C>T).
Li et al., "MicroRNA-25 promotes gastric cancer proliferation, invasion, and migration by directly targeting F-box and WD-40 Domain Protein 7, FBXW7," Tumor Biology, vol.
Tested genes include ABL1, AKT1, ALK, APC, ATM, BRAF, CDH1, CDKN2A, CSF1R, CTNNB1, EGFR, ERBB2, ERBB4, EZF2, FBXW7, FGFR1, FGFR2, FGFR3, FLT3, GNA11, GNAQ, GNAS, HNF1A, HRAS, IDH1, IDH2, JAK2, JAK3, KDR, KIT, KRAS, MET, MLH1, MPL, NOTCH1, NPM1, NRAS, PDGFRA, PIK3CA, PTEN, PTPN11, RB1, RET, SMAD4, SMARCB1, SMO, SRC, STK11, TP53, and VHL.
In the Next-Generation Sequencing Solid Tumor Survey (NGSST-A-2016), 111 laboratories were provided blinded specimens containing 10 recurrent somatic SNVs in AKT1, ALK, BRAF, EGFR, FBXW7, IDH1, KIT, KRAS, NRAS, and PIK3CA, with a variant allele fraction between 15% and 50%.
This laboratory-developed NGS test protocol is based on a well-validated research use-only kit that targets 54 genes, including all exons of 15 genes (BCOR, BCORL1, CDKN2A, CEBPA, CUX1, DNMT3A, ETV6, EZH2, IKZF1, KDM6A, PHF6, RAD21, RUNX1, STAG2, and ZRSR2) and hot spot exons/regions of 39 genes (ABL1, ASXL1, ATRX, BRAF, CALR, CBL, CBLB, CBLC, CSF3R, FBXW7, FLT3, GATA1, GATA2, GNAS, HRAS, IDH1, IDH2, JAK2, JAK3, KIT, KMT2A/MLL, KRAS, MPL, MYD88, NOTCH1, NPM1, NRAS, PDGFRA, PTEN, PTPN11, SETBP1, SF3B1, SMC1A, SMC3, SRSF2, TET2, TP53, U2AF1, and WT1).
It uses 10 ng of DNA to analyze more than 2800 mutations across 50 known oncogenes and tumor suppressor genes including ABL1, AKT1, ALK, APC, ATM, BRAF, CDH1, CDKN2A, CSF1R, CTNNB1, EGFR, ERBB2, ERBB4, EZH2, FBXW7, FGFR1, FGFR2, FGFR3, FLT3, GNA11, GNAS, GNAQ, HNF1A, HRAS, IDH1, IDH2, JAK2, JAK3, KDR, KIT, KRAS, MET, MLH1, MPL, NOTCH1, NPM1, NRAS, PDGFRA, PIK3CA, PTEN, PTPN11, RB1, RET, SMAD4, SMARCB1, SMO, SRC, STK11, TP53, and VHL.
The primers used target 207 hotspots covering 50 genes: ABL1, AKT1, ALK, APC, ATM, BRAF, CDH1, CDKN2A, CSF1R, CTNNB1, EGFR, ERBB2, ERBB4, EZF2, FBXW7, FGFR1, FGFR2, FGFR3, FLT3, GNA11, GNAQ, GNAS, HNF1A, HRAS, IDH1, IDH2, JAK2, JAK3, KDR, KIT, KRAS, MET, MLH1, MPL, NOTCH1, NPM1, NRAS, PDGFRA, PIK3CA, PTEN, PTPN11, RB1, RET, SMAD4, SMARCB1, SMO, SRC, STK11, TP53, and VHL (Ion AmpliSeq Cancer Hopspot Panel v2; Life Technologies).
Many other genes are commonly mutated in CLL, including the following: NOTCH1; XPO1 (exportin 1); MYD88; KLH6 (Kelch-like 6); TP53; TGM; BIRC3; PLEKHG5; ATM; SF3B1 (splicing factor 3, B1 unit); ZMYM3; MAPK1; FBXW7; and DDX3X.
The most-common, potentially targetable alterations were mutations, amplifications, and homozygous deletions of PIK3CA (n = 8; 40%), PTEN (n = 5; 25%), CDKN2A/B (n = 4; 20%), CCND3 (n = 3; 15%), CCNE1 (n = 2; 10%), and EGFR (n = 2; 10%), with AKT3, CCND1, CCND2, CDK4, FBXW7, FGFR1, HRAS, NF1, PIK3R1, and SRC altered in a single case (Figure 1; Table 1).
The panel contains probes to generate 212 amplicons from 48 cancer-related genes: ABL1, AKT1, ALK, APC, ATM, BRAF, CDH1, CDKN2A, CSF1R, CTNNB1, EGFR, ERBB2, ERBB4, FBXW7, FGFR1, FGFR2, FGFR3, FLT3, GNA11, GNAQ, GNAS, HNF1A, HRAS, IDH1, JAK2, JAK3, KDR, KIT, KRAS, MET, MLH1, MPL, NOTCH1, NPM1, NRAS, PDGFRA, PIK3CA, PTEN, PTPN11, RB1, RET, SMAD4, SMARCB1, SMO, SRC, STK11, TP53, and VHL.