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At least 469 records · Page 26Linked to original sources
PubMed2000

Effects of factor V gene G1691A, methylenetetrahydrofolate reductase gene C677T, and prothombin gene G20210A mutations on deep venous thrombogenesis in Behçet's disease.

OBJECTIVE: Behçet's disease (BD) is a multisystemic disease of unknown etiology, characterized by aphthous ulcerations and uveitis, that is common in the Turkish population. Venous involvement is observed in 25% of the cases. While superficial thrombophlebitis is the most common finding, deep venous thrombosis (DVT) follows it. Hyperactivity in the coagulation pathway, hypoactive anticoagulation mechanisms, or faulty fibrinolysis generate a tendency for thrombogenesis. Mutations of the genes involved in these pathways may cause predisposition to thrombosis. METHODS: Possible roles of methylenetetrahydrofolate reductase (MTHFR) gene C677T, factor V (FV) gene G1691A (Leiden), and prothrombin gene G20210A polymorphisms in venous thrombogenesis were evaluated in patients with BD; 100 healthy people, 30 BD patients without DVT, 30 BD patients with DVT, and 30 patients with idiopathic DVT were studied with the restriction fragment length polymorphism method for these 3 polymorphisms. The frequencies of these mutations for each group, separately and in combinations, are described. RESULTS: Among the 3 mutations, FV Leiden mutation was found to be a risk factor for DVT. An association between FV Leiden mutation and BD was likely, but FV Leiden mutation did not increase the risk for deep venous thrombogenesis in BD patients. MTHFR gene C677T mutation does not increase risk of DVT in BD either alone or combined with FV Leiden mutation. CONCLUSION: Although a thrombotic tendency is one of the major characteristics of BD, we found no association between these 3 thrombogenetic mutations and BD patients with thromboses.

Adolescent↗
PubMed1987

The cellular retinol binding protein II gene. Sequence analysis of the rat gene, chromosomal localization in mice and humans, and documentation of its close linkage to the cellular retinol binding protein gene.

Cellular retinol binding protein II (CRBP II) is an abundant, 134-residue protein present in the small intestinal epithelium. It is thought to participate in the uptake and/or intracellular metabolism of vitamin A. We have isolated and sequenced the rat CRBP II gene. Its four exons span 0.65 kilobases and are interrupted by three introns with an aggregate length of 19.5 kilobases. Southern blot hybridization analysis indicated that this gene is highly conserved in rats, mice, and humans. CRBP II belongs to a protein family that contains eight known members. Computer-assisted comparative sequence analyses indicated that a region of internal homology spans its first two exons and that oligopeptide domains specified by these first two exons exhibit significant homology to all other family members as well as to a portion of the all-trans-retinol binding domain that has previously been defined in serum retinol binding protein. The CRBP II gene was mapped in mice using recombinant inbred strains and restriction fragment length polymorphisms. It is located on chromosome 9 within 5.3 centimorgans of the phosphoglucomutase-3 locus and is closely linked (within 3.0 centimorgans) to the gene specifying a highly homologous intracellular retinol binding protein known as CRBP. Mouse-human somatic cell hybrids were used to determine that both the CRBP and CRBP II genes are located on human chromosome 3.

Amino Acid Sequence↗
PubMed1998

Characterization of the mouse PA28 activator complex gene family: complete organizations of the three member genes and a physical map of the approximately 150-kb region containing the alpha- and beta-subunit genes.

The proteasome is a multisubunit protease responsible for the generation of peptides loaded onto MHC class I molecules. Recent evidence indicates that binding of an IFN-gamma-inducible PA28 activator complex to the 20S proteasome enhances the generation of class I binding peptides. The alpha- and beta-subunits, which constitute the PA28 activator complex in the form of an (alphabeta)3 heterohexamer, show significant amino acid sequence similarity to a protein, designated Ki or the gamma-subunit, that is capable of binding to the 20S proteasome. In this study, we describe the complete nucleotide sequences of the mouse genes, Psme1, Psme2, and Psme3, coding for the alpha-, beta-, and gamma-subunits, respectively. The overall exon-intron organizations of the three Psme genes are virtually identical, thus providing evidence that they are descended from a single ancestral gene. The promoter regions of the Psme1 and Psme2 genes contain sequence motifs that qualify as IFN-stimulated response elements, consistent with the observation that their expression is induced strongly by IFN-gamma. The Psme1 and Psme2 genes are located approximately 6 kb apart with their 3'-ends pointing toward each other on bands C2 to D1 of mouse chromosome 14, supporting the idea that they emerged by tandem duplication.

Amino Acid Sequence↗
PubMed2000

Functional analysis of six genes from chromosomes XIV and XV of Saccharomyces cerevisiae reveals YOR145c as an essential gene and YNL059c/ARP5 as a strain-dependent essential gene encoding nuclear proteins.

We report here basic functional analysis of strains deleted for six open reading frames (ORFs), YNL059c and YNL148c from chromosome XIV and YOR145c, YOR152c, YOR161c and YOR162c from chromosome XV of Saccharomyces cerevisiae. ORFs were replaced with the KanMX4 resistance marker using a long flanking homology PCR strategy in FY1679 and W303 diploid strains. Replacement cassettes were constructed in plasmid pUG7 and the cognate wild-type genes were recovered by gap repair. Sporulation and tetrad analysis revealed that deletion of YNL059c/ARP5 was lethal for vegetative growth in strain W303 and caused severe growth defects in strain FY1679 while YOR145c was essential for growth in both strains. Fusion of the green fluorescent protein (GFP) gene to the 3' ends of the YNL059c/ARP5 and YOR145c coding sequences created functional chimeric genes at the respective chromosomal loci. Both Arp5-GFP and Yor145-GFP localized to the nucleus, Yor145-GFP concentrating in the nucleolus. The vectors containing the deletion cassettes and the cognate wild-type genes, the oligonucleotides, and the deletant strains are available from the EUROFAN resource centre EUROSCARF (Frankfurt).

Actins↗
PubMed1994

A four base pair deletion 5' to the A gamma T gene is associated not only with decreased expression of the A gamma T-globin gene, but also of the G gamma-globin gene in cis.

A four base pair deletion 5' to A gamma T-globin gene at positions -222 to -225 has been reported to reduce the expression of this gene. To evaluate the prevalence and effect of this deletion, PCR-based methods were employed. The deletion had a gene frequency of 0.06 in a sample of African-American individuals with sickle cell trait, 0.18 in adult African-Americans with normal Hb AA, and 0.36 in caucasians. Seventy cord blood samples from African-American newborns with Hb AA were evaluated by both HPLC and PCR. The frequency of the A gamma T allele was 0.13. The A gamma T-globin chain was always present in a lower proportion than the A gamma I allele (70% of A gamma I), but the percentage of A gamma-globin was the same whether or not A gamma T was present. The total percentage of Hb F, however, was significantly lower in the group with the A gamma T allele (77.1% vs. 87.4%, P < 0.01). These results indicate that the four base pair deletion is not only associated with reduced expression of the A gamma T allele, but also of the G gamma allele in cis, further suggesting a possible role of this region in the modulation of the expression of the linked gamma-globin genes.

Base Sequence↗
PubMed2006

Nitric oxide differentially regulates the gene expression of caspase genes but not some autophagic genes.

Nitric oxide (NO) is fundamentally important molecule which produces a wide range of cellular effects with the most poorly understood one being alteration in the sensitivity to cell death. The objective of this study was to test the hypothesis that NO would differentially affect caspase or autophagy gene expression in a manner that might account for the disparate actions of NO to either enhance or protect against cell death. Neonatal mouse cardiomyocytes in culture were treated with the NO donor SIN-1 (3-morpholinosydnonimine hydrochloride) for up to 20 h. RNA was collected, after either 2, 4 or 20 h, labeled and hybridized to cDNA microarray slides The concentration of SIN-1 was selected after concentration response studies of SIN-1 on cell viability, assessed by the MTT assay. The cDNA microarrays were used that contained the mouse genome version 2.0 with genes for enzymes crucial to apoptosis, namely caspases-1, -2, -3, -6, -7, -8, -9, -11, -12 and -14, as well as for enzymes crucial to autophagy namely beclin-1, Apg5l and Apg12l. Considering the entire 20 h period, treatment with SIN-1 was associated with significant (p<0.05) changes in five caspases. In contrast, there were no changes in the three separate genes involved in autophagy. Time course experiments showed a consistent increase in caspase-8, -11 and -14, and a consistent decrease in caspase-1 and -6. Notably, caspase-1 showed a persistent and marked reduction so that after 20 h of treatment, caspase-1 was dramatically reduced, almost ten fold, to 0.14+/-0.11 of control. In conclusion, these results suggest that: (i) NO regulates the expression of genes involved in apoptotic but not some involved in autophagic cell death; (ii) the more recently discovered caspase-14 may have a role in the heart; (iii) NO-induced alteration of different caspases may explain the ability of NO to either enhance or protect against cell death depending on whether associated factors involve, respectively caspases-8, -11, and -14 or -1 and -6.

Animals↗
PubMed2000

Combined suicide gene therapy for human colon cancer cells using adenovirus-mediated transfer of escherichia coli cytosine deaminase gene and Escherichia coli uracil phosphoribosyltransferase gene with 5-fluorocytosine.

The virus-directed enzyme/prodrug system using the Escherichia coli cytosine deaminase (CD) gene and 5-fluorocytosine (5-FC) suffers from a sensitivity limitation in many tumor cells. The E. coil uracil phosphoribosyltransferase (UPRT), which is a pyrimidine salvage enzyme, directly converts 5-fluorouracil (5-FU) to 5-fluorouridine monophosphate at the first step of its activating pathway. To improve the antitumoral effect of the CD/5-FC system, we investigated a combined suicide gene transduction therapy for human colon cancer cells using two separate adenovirus vectors expressing the E. coli CD and E. coli UPRT genes and systemic 5-FC administration (the CD, UPRT/5-FC system). The present study demonstrates that the CD, UPRT/5-FC system generates a co-operative effect of CD and UPRT, resulting in dramatic increases in both RNA- and DNA-directed active forms, including 5-fluorouridine triphosphate incorporated into RNA, 5-fluorodeoxyuridine monophosphate, and the thymidylate synthase inhibition rate, compared with the CD/5-FC system. Furthermore a significant increase in the 5-FC sensitivity of colon cancer cells was demonstrated in the CD, UPRT/5-FC system compared with the CD/5-FC system in vitro and in vivo. These results suggest that the CD, UPRT/5-FC system is a powerful approach in gene therapy for colorectal cancer.

Adenoviridae↗
PubMed1998

Expression of the Elm1 gene, a novel gene of the CCN (connective tissue growth factor, Cyr61/Cef10, and neuroblastoma overexpressed gene) family, suppresses In vivo tumor growth and metastasis of K-1735 murine melanoma cells.

We previously isolated a partial cDNA fragment of a novel gene, Elm1 (expressed in low-metastatic cells), that is expressed in low-metastatic but not in high-metastatic K-1735 mouse melanoma cells. Here we determined the full-length cDNA structure of Elm1 and investigated the effect of Elm1 expression on growth and metastatic potential of K-1735 cells. The Elm1 gene encodes a predicted protein of 367 amino acids showing approximately 40% amino acid identity with the CCN (connective tissue growth factor [CTGF], Cyr61/Cef10, neuroblastoma overexpressed gene [Nov]) family proteins, which consist of secreted cysteine-rich proteins with growth regulatory functions. Elm1 is also a cysteine-rich protein and contains a signal peptide and four domains conserved in the CCN family proteins. Elm1 was highly conserved, expressed ubiquitously in diverse organs, and mapped to mouse chromosome 15. High-metastatic K-1735 M-2 cells, which did not express Elm1, were transfected with an Elm1 expression vector, and several stable clones with Elm1 expression were established. The in vivo growth rates of cells expressing a high level of Elm1 were remarkably slower than those of cells expressing a low level of Elm1. Metastatic potential of transfectants was reduced in proportion to the level of Elm1 expression. Thus, Elm1 is a novel gene of CCN family that can suppress the in vivo growth and metastatic potential of K-1735 mouse melanoma cells.

Animals↗
PubMed1993

Mitochondrial genes in the colourless alga Prototheca wickerhamii resemble plant genes in their exons but fungal genes in their introns.

The mitochondrial DNA from the colourless alga Prototheca wickerhamii contains two mosaic genes as was revealed from complete sequencing of the circular extranuclear genome. The genes for the large subunit of the ribosomal RNA (LSUrRNA) as well as for subunit I of the cytochrome oxidase (coxI) carry two and three intronic sequences respectively. On the basis of their canonical nucleotide sequences they can be classified as group I introns. Phylogenetic comparisons of the coxI protein sequences allow us to conclude that the P.wickerhamii mtDNA is much closer related to higher plant mtDNAs than to those of the chlorophyte alga C.reinhardtii. The comparison of the intron sequences revealed several unusual features: (1) The P.wickerhamii introns are structurally related to mitochondrial introns from various ascomycetous fungi. (2) Phylogenetic analyses indicate a close relationship between fungal and algal intronic sequences. (3) The P. wickerhamii introns are located at positions within the structural genes which can be considered as preferred intron insertion sites in homologous mitochondrial genes from fungi or liverwort. In all cases, the sequences adjacent to the insertion sites are very well conserved over large evolutionary distances. Our finding of highly similar introns in fungi and algae is consistent with the idea that introns have already been present in the bacterial ancestors of present day mitochondria and evolved concomitantly with the organelles.

Amino Acid Sequence↗
PubMed2001

EMF genes interact with late-flowering genes in regulating floral initiation genes during shoot development in Arabidopsis thaliana.

To investigate the mechanisms regulating the initiation of floral development in Arabidopsis, a construct containing beta-glucuronidase (GUS) gene driven by APETALA1 promoter (AP1::GUS) was introduced into emf fwa and emf ft double mutants. GUS activity was strongly detected on shoot meristem of emf1-1 single mutants harboring AP1::GUS construct just 5 d after germination. By contrast, GUS activity was undetectable on emf1-1 fwa-1, emf1-1 ft-1, emf2-1 fwa-1, emf2-3 fwa-1 and emf2-3 ft-1 double mutants harboring AP1::GUS construct 10 d after germination. GUS activity was only weakly detected on the apical meristem of 20-day-old emf1-1 fwa-1 and emf2-1 fwa-1 seedlings. During this time, only sessile leaves were produced. Further analysis indicated that AP1 was strongly expressed in 10-day-old emf1-1 and emf2-1 single mutants. Its expression was significantly reduced in all emf1-1 or emf2-1 late-flowering double mutants tested. Similar to AP1, the expression of LEAFY (LFY) was also high in emf1-1 and emf2-1 single mutants and reduced in emf1-1 or emf2-1 late-flowering double mutants. Our results indicate that the precocious expression of AP1 and LFY is dependent not only on the low EMF and FWA activities but also on the expression of most of the late-flowering genes such as FT, FCA, FE, CO and GI. These data also reveal that most late-flowering genes may function downstream of EMF or in pathways distinct from EMF to activate genes specified floral meristem identity during shoot maturation in Arabidopsis.

Alleles↗
PubMed2006

Virus-induced gene silencing of argonaute genes in Nicotiana benthamiana demonstrates that extensive systemic silencing requires Argonaute1-like and Argonaute4-like genes.

Several distinct pathways of RNA silencing operate in plants with roles including the suppression of virus accumulation, control of endogenous gene expression, and direction of DNA and chromatin modifications. Proteins of the Dicer-Like and Argonaute (AGO) families have key roles within these silencing pathways and have distinct biochemical properties. We are interested in the relationships between different silencing pathways and have used Nicotiana benthamiana as a model system. While not being an amenable plant for traditional genetics, N. benthamiana is extensively used for RNA-silencing studies. Using virus-induced gene silencing technology we demonstrate that both NbAGO1- and NbAGO4-like genes are required for full systemic silencing but not for silencing directed by an inverted repeat transgene. Phenotypic differences between the virus-induced gene silencing plants indicate that NbAGO1 and NbAGO4 like act at different stages of the silencing pathways. Suppression of NbAGO1 expression recapitulated the hypomorphic mutant phenotype of certain Arabidopsis (Arabidopsis thaliana) ago1 alleles, however, suppression of NbAgo4 like resulted in phenotypes differing in some respects from those reported for Arabidopsis ago4. We suggest that the small interfering RNA amplification step required for full systemic silencing is dependent upon a nuclear event requiring the activity of NbAGO4 like.

Amino Acid Sequence↗
PubMed1990

Molecular analysis of two genes of the Escherichia coli gab cluster: nucleotide sequence of the glutamate:succinic semialdehyde transaminase gene (gabT) and characterization of the succinic semialdehyde dehydrogenase gene (gabD).

We have characterized two genes of the Escherichia coli K-12 gab cluster, which encodes the enzymes of the 4-aminobutyrate degradation pathway. The nucleotide sequence of gabT, coding for glutamate:succinic semialdehyde transaminase (EC 2.6.1.19), alternatively known as 4-aminobutyrate transaminase, was determined. The structural gene consists of 1,281 nucleotides specifying a protein of 426 amino acids with a molecular mass of 45.76 kDa. The protein shows significant homologies to the ornithine transaminases from Saccharomyces cerevisiae and from rat and human mitochondria. Three functionally and structurally important amino acid residues of the transaminase were identified by sequence comparison studies, and evolutionary relationships of the aminotransferases are discussed. The gabD gene, encoding succinic semialdehyde dehydrogenase (EC 1.2.1.16), was cloned and shown to be located adjacent to the 5' end of gabT. Expression studies with subfragments of the initially cloned DNA region revealed a maximal size of 1.7 kb for gabD. Both genes are cotranscribed from a promoter located upstream of gabD.

4-Aminobutyrate Transaminase↗
PubMed2001

Screening of environmental DNA libraries for the presence of genes conferring Na(+)(Li(+))/H(+) antiporter activity on Escherichia coli: characterization of the recovered genes and the corresponding gene products.

Environmental DNA libraries prepared from three different soils were screened for genes conferring Na(+)(Li(+))/H(+) antiporter activity on the antiporter-deficient Escherichia coli strain KNabc. The presence of those genes was verified on selective LK agar containing 7.5 mM LiCl. Two positive E. coli clones were obtained during the initial screening of 1,480,000 recombinant E. coli strains. Both clones harbored a plasmid (pAM1 and pAM3) that conferred a stable Li(+)-resistant phenotype. The insert of pAM2 (1,886 bp) derived from pAM1 contained a gene (1,185 bp) which encodes a novel Na(+)/H(+) antiporter belonging to the NhaA family. The insert of pAM3 harbored the DNA region of E. coli K-12 containing nhaA, nhaR, and gef. This region is flanked by highly conserved insertion elements. The sequence identity with E. coli decreased significantly outside of the insertion sequence elements, indicating that the unknown organism from which the insert of pAM3 was cloned is different from E. coli. The products of the antiporter genes located on pAM2 and pAM3 revealed functional homology to NhaA of E. coli and enabled the antiporter-deficient E. coli mutant to grow on solid media in the presence of up to 450 mM NaCl or 250 mM LiCl at pH 8.0. The Na(+)/H(+) antiporter activity in everted membrane vesicles that were derived from the E. coli strains KNabc/pAM2 and KNabc/pAM3 showed a substantial increase between pHs 7 and 8.5. The maximal activity was observed at pHs 8.3 and 8.6, respectively. The K(m) values of both antiporters for Na(+) were approximately 10-fold higher than the values for Li(+).

Amino Acid Sequence↗
PubMed2000

[Construction of gene targeting vector for duplicating p35Nck5a gene and its application in the gene targeting of ES cells].

To duplicating the regulatory subunit p35Nck5a gene of mouse neuronal cdc2-like kinase in embryonic stem (ES) cells, about 12.2 kb of pGDTV vector for p35Nck5a gene duplication was constructed. The linearized pGDTV vectors were transfected into ES cells by electroporation. 245 drug-resistant cell clones were obtained in both G418 and GANC medium and the frequency of surviving cells was 6.22 x 10(-5). The ES cell clones were identified to have duplicated the p35Nck5a gene by use of both PCR and genomic Southern blotting, and the frequency of homologous recombination is 5.08 x 10(-7). The use of negative selection gene (HSV-tk) results in 7-fold increase at selection efficiency. This study lays the foundations of preparing mouse models of Alzheimer's disease.

Alzheimer Disease↗
PubMed1964

ON THE RELATIONSHIPS BETWEEN THE GAMMA-GLOBULIN GENES OF THE GM SYSTEM. A STUDY OF GM GENE PRODUCTS IN SERA, MYELOMA GLOBULINS, AND SPECIFIC ANTIBODIES WITH SPECIAL REFERENCE TO THE GENE GM.

Gm types of sera from Caucasians and Negroes, of myeloma globulins, and of specific antibodies were investigated. In particular the relationship between the recently identified gene Gm(f) and other Gm genes was analyzed. 1. Caucasians were, with rare exceptions, either Gm(b+f+) or Gm(b-f-). 2. In Negroes, on the other band, type Gm(b+f-) was found to be common. 3. No myeloma globulins appeared to contain the product of more than 1 of the 3 genes Gm(a), Gm(b), and Gm(f), even though the large majority of normal individuals, as well as myeloma patients, possess 2 or all 3 of these genes. 4. The types Gm(a+b-f-) and Gm(a-b-f+) represented the 2 major groups among the gamma(2)-myeloma globulins; each comprised roughly 40 per cent. The types Gm(a- b+f-) and Gm(a-b-f-) are minor groups. 5. All Gm(x+) myeloma globulins were also Gm(a+). Approximately half of the Gm(a+) myeloma globulins were Gm(x+). 6. In the majority, but not in all, of Gm(a+) sera the anti-Rh antibodies were clearly Gm(a+). Similarly, the anti-Rh antibodies of Gm(f+) sera were most often, but not always, also Gm(f+). In contrast, only a minor proportion of Gm(b+) anti-Rh sera sensitized red cells to anti-Gm(b).

Antibodies↗
PubMedDate not supplied

Proto-oncogenes, growth factor genes, receptor genes, differentiation genes and structural rearrangements in human cancer.

Information on chromosomal structural rearrangements in leukemia and solid tumors was retracted from a computerized databank and the literature. A binomial test procedure was used to determine the statistical significance of the observed numbers of breaks. Some 131 human cancer-specific chromosomal structural rearrangements were also taken from the literature. The results showed that breakage and deletion occurred preferentially in bands known to contain proto-oncogenes, growth factor genes, receptor genes and differentiation genes. Therefore, chromosomal structural rearrangements could be used to find and map new genes involved in the genesis and/or progression of neoplasia.

Cell Differentiation↗
PubMed2002

High-level erythroid lineage-directed gene expression using globin gene regulatory elements after lentiviral vector-mediated gene transfer into primitive human and murine hematopoietic cells.

Lentiviral vectors efficiently transduce primitive human hematopoietic cells and are capable of transferring complex genomes. Vectors were designed with hypersensitive sites containing regulatory elements from the beta-globin locus control region linked to the beta-globin gene promoter to drive expression of the enhanced green fluorescent protein marker to facilitate analysis of the pattern of gene expression in various hematopoietic lineages. Such vectors gave higher level, induced expression in mouse erythroleukemia cells than a previously described vector that utilized an enhancer from the alpha locus and the ankyrin-1 promoter [Moreau-Gaudry, F., Xia, P., Jiang, G., Perelman, N.P., Bauer, G., Ellis, J., Surinya, K.H., Mavilio, F., Shen, C.K., and Malik, P. (2001). Blood 98, 2664-2672]. The addition of gamma-globin intron sequences further augmented vector expression. Expression was also effectively targeted to the erythroid lineage in cultured human cells from peripheral blood and in mouse red blood cells in vivo, although lower levels of expression were also observed in other lineages. Thus, these newly described vectors provide a means to achieve high-level gene expression, predominantly in erythroid cells, an outcome that may have potential therapeutic application.

Animals↗
PubMed1994

The yeast MOT2 gene encodes a putative zinc finger protein that serves as a global negative regulator affecting expression of several categories of genes, including mating-pheromone-responsive genes.

The STE4 gene encodes the beta subunit of a heterotrimeric G protein that is an essential component of the pheromone signal transduction pathway. To identify downstream component(s) of Ste4, we sought pseudo-revertants that restored mating competence to ste4 mutants. The suppressor mot2 was isolated as a recessive mutation that restored conjugational competence to a temperature-sensitive ste4 mutant and simultaneously conferred a temperature-sensitive growth phenotype. The MOT2 gene encodes a putative zinc finger protein, the deletion of which resulted in temperature-sensitive growth, increased expression of FUS1 in the absence of pheromones, and suppression of a deletion of the alpha-factor receptor. On the other hand, sterility resulting from deletion of STE4 was not suppressed by the mot2 deletion. These phenotypes are similar to those associated with temperature-sensitive mutations in CDC36 and CDC39, which are proposed to encode general negative regulators of transcription rather than factors involved in the pheromone response pathway. Deletion of MOT2 also caused increased transcription of unrelated genes such as GAL7 and PHO84. Overexpression of MOT2 suppresses the growth defect of temperature-sensitive mutations in CDC36 and CDC39. These observations suggest that Mot2 functions as a general negative regulator of transcription in the same processes as Cdc36 and Cdc39.

Amino Acid Sequence↗