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Example sentences for: fhit
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3 region to which RASSF1A maps undergoes deletions in many solid tumor types, including GCTs [ 9 ] . RASSF1A encodes a splice variant of human RAS effector homologue, which interacts with the XPA protein and functions as a negative regulator of cell growth [ 16 17 ] . RASSF1A has been shown to be inactivated by promoter methylation in a variety of tumor types [ 16 17 18 19 ] . The 17q21 and 17p13 regions, to which BRCA1 and HIC1 map, respectively, also have been characterized by high frequency of LOH in GCT [ 9 ] . The BRCA 1 gene plays critical roles in DNA repair and recombination, cell cycle checkpoint control, and transcription and has been shown to be hypermethylated in breast-ovarian cancer [ 4 ] . The HIC1 gene is also often hypermethylated in many human cancers [ 20 21 22 ] . The DNA repair gene MGMT encodes O(6)-methylguanine-DNA methyltransferase and this enzyme effectively removes DNA adducts formed by alkylating agents [ 23 ] . Epigenetic inactivation of the MGMT gene was reported in a wide variety of cancers [ 24 25 ] . Also, a low frequency of methylation of the APC , RARB , and FHIT genes was detected in NSGCTs.
An added benefit of these constructions is the availability of yeast strains that possess high levels of dinucleoside polyphosphates and at the same time express a mutant Fhit-homologous protein, because these are conditions which have been postulated to constitute the signaling form of Fhit [ 16 ] . Finally, using controlled genotypes we revisited conditions that lead to increased accumulation of dinucleoside polyphosphates [ 24 25 26 27 28 29 30 31 32 33 ] . Recognizing that hnt2 deletion is a pathological condition, we were particular interested in identifying conditions that lead to accumulation of such compounds in cells that contain a functional HNT2 gene, rather than simply identifying conditions that produce diadenosine polyphosphate accumulation in the absence of Hnt2.
The human FHIT gene, located at the chromosome 3 fragile site FRA3B, is inactivated early in the development of many tumors [ 1 ] . Murine Fhit is also located at a fragile site [ 2 3 ] and mice heterozygous for disruption of Fhit , given low intragastric doses of the mutagen N-nitrosomethylbenzylamine, develop stomach and sebaceous tumors [ 4 ] that can be prevented by viral Fhit expression [ 5 ] . Fhit, a dimer of 147 amino acid subunits, is a member of the histidine triad (HIT) superfamily of nucleotide hydrolases and transferases [ 6 7 ] . Members of the Hint branch of the HIT superfamily are found in all forms of life [ 8 ] . The S. cerevisiae Hint homolog, Hnt1, and rabbit Hint possess adenosine monophosphoramidase activity that functions in yeast to positively regulate function of Kin28, Ccl1 and Tfb3, which constitute the kinase component of general transcription factor TFIIH [ 9 ] . A new Hint related protein, Aprataxin, is mutated in individuals with ataxia with oculomotor apraxia [ 10 11 ] and has a yeast homolog termed Hnt3 [ 9 ] . Members of the Fhit branch of the HIT superfamily have been found in fungi [ 12 13 ] , animals [ 2 14 15 ] and plants [ 7 ] and hydrolyze diadenosine tetraphosphate, diadenosine triphosphate and other 5'-5"'-dinucleoside polyphosphates.
Sodium salts of each compound were titrated into assays of purified Fhit [ 16 ] with 1.8 μM fluorescent substrate, Appp-S-(4-4-difluoro-5,7-dimethyl-4-bora-3a,4a-diaza-s-indacine-3-yl)methylaminoacetyl (ApppBODIPY) [ 10 ] , and competitive K i values were obtained by calculating the inhibitor concentration-dependence in reduction of k cat / K m (apparent) for substrate hydrolysis [ 10 ] . As shown in Table 1, inhibitors 2b and 3b with two-carbon diol linkers were either only as inhibitory as the natural substrate 1 or substantially less so.
Derivatives of pentaerythritol, tetrapodal compounds 12,13 and 14, were also evaluated for Fhit inhibition.
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