ライフサイエンスコーパス: FANCF

1 FANCF inactivation in ovarian tumors resulted from methy

2 FANCF methylation was associated with a shorter duration

3 FANCF mutants bearing amino acid substitutions in this C

4 FANCF-deregulated CC cell lines also exhibit a chromosom

5 ANCB (3), FANCC (3), FANCD1 (1), FANCD2 (3), FANCF (2), FANCG (2), FANCI (1), FANCJ (2), and FANCL (3

6 We identify a FANCF promoter cis element, which is activated by ICSBP

7 In addition, FANCF methylation was found in one cell line by screenin

8 n motifs that bind to SH3 domains, FANCC and FANCF, did not interact with the SH3 domain of alphaIISp

9 FANCA, FANCC, FANCG, and FANCF proteins form a multisubunit nuclear complex (FA c

10 CA significantly reduced MMC sensitivity but FANCF, FANCG, and FANCC did not.

11 initial methylation of FANCF is followed by FANCF demethylation and ultimately results in cisplatin

12 o methylation was observed for APAF-1, DAPK, FANCF, FAS, P14, P21, P73, SOCS-3, and SURVIVIN.

13 Using siRNA to knock down FANCF in 8226/LR5 and U266/LR6 drug-resistant cells demo

14 es, we identify the gene encoding Fanconi F (FANCF) as an ICSBP target gene.

15 al genes in the FA pathway, including FANCA, FANCF, FANCL, FANCD2, BRCA1, and BRCA2, are required for

16 analysis to determine whether FANCA, FANCC, FANCF, and FANCG directly interact with ERCC1 and XPF an

17 nuclear complex containing the FANCA, FANCC, FANCF, and FANCG proteins is required for the activation

18 y related profiles to miR-210: BRCA1, FANCD, FANCF, PARP1, E-cadherin, and Rb1 were all activated in

19 ciated proteins (FANCA, FANCB, FANCC, FANCE, FANCF, FANCG and FANCL) form a nuclear Fanconi anemia co

20 The FA proteins FANCA, FANCC, FANCE, FANCF, FANCG, and FANCL participate in a core complex.

21 Fanconi anemia (FANCA, FANCC, FANCD2, FANCE, FANCF and FANCG) as well as BRCA1 and BRCA2 (FANCD1).

22 gene products (FANCA, FANCC, FANCD2, FANCE, FANCF, and FANCG proteins) interact in a common pathway.

23 least 6 genes (FANCA, FANCC, FANCD2, FANCE, FANCF, and FANCG).

24 (FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, and FANCL), and identified orthologs in th

25 (FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ, FANCL, FANCM, and FANCN).

26 s: NRG1, DOCK10, GLS, PRPS1, TMEM161B, GLO1, FANCF, HNRNPDL, CD47, OLFM1, SMAD7, and SLC6A4.

27 nd the FANCF protein, as well as a 43-kd His-FANCF fusion protein lacking the antibody motif, in Esch

28 ing or internalization was observed with His-FANCF.

29 The human FANCF protein reportedly functions as a molecular adapto

30 methylation and histone deacetylases induces FANCF gene re-expression in CC cell lines.

31 In adenocarcinomas of the lung, FANCF promoter methylation was a significant predictor o

32 chromosome 3 near ZNF659, chromosome 11 near FANCF, chromosome 11 near ZBTB15, and chromosome 12 near

33 resistance correlated with demethylation of FANCF.

34 ographic studies of the C-terminal domain of FANCF reveal a helical repeat structure similar to the C

35 CG, we now demonstrate direct interaction of FANCF with FANCG, of FANCC with FANCE and a weaker inter

36 stent with the known nuclear localization of FANCF.

37 Two C-terminal loops of FANCF are essential for monoubiquitination of FANCD2 and

38 gression in which the initial methylation of FANCF is followed by FANCF demethylation and ultimately

39 Promoter methylation of FANCF occurred in 15% (13/89) of HNSCCs and 14% (22/158)

40 Overexpression of FANCF in 8226/S and U266/S drug-sensitive cells partiall

41 Here, we show that FANCF gene is disrupted by either promoter hypermethylat

42 ntibody to the myeloid antigen CD33, and the FANCF protein, as well as a 43-kd His-FANCF fusion prote

43 The recent cloning of the FANCF and FANCE genes has allowed us to investigate the

44 BRCA pathway via promoter methylation of the FANCF gene renders cells sensitive to DNA crosslinking a

45 racts with the FA core complex by binding to FANCF, whereas MM2 interacts with RM1 and topoisomerase

46 nclusion: DNA repair defects associated with FANCF deficiency do not prohibit CRISPR/Cas9 gene correc

47 restored by functional complementation with FANCF, a gene that is upstream in this pathway.