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Journal articles on the topic 'Global suppressor'

Author: Grafiati

Published: 6 September 2023

Last updated: 31 July 2025

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1

Chattopadhyay, Gopinath, Jayantika Bhowmick, Kavyashree Manjunath, Shahbaz Ahmed, Parveen Goyal, and Raghavan Varadarajan. "Mechanistic insights into global suppressors of protein folding defects." PLOS Genetics 18, no. 8 (2022): e1010334. http://dx.doi.org/10.1371/journal.pgen.1010334.

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Most amino acid substitutions in a protein either lead to partial loss of function or are near neutral. Several studies have shown the existence of second-site mutations that can rescue defects caused by diverse loss of function mutations. Such global suppressor mutations are key drivers of protein evolution. However, the mechanisms responsible for such suppression remain poorly understood. To address this, we characterized multiple suppressor mutations both in isolation and in combination with inactive mutants. We examined six global suppressors of the bacterial toxin CcdB, the known M182T gl

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2

Shortle, David, and Beth Lin. "GENETIC ANALYSIS OF STAPHYLOCOCCAL NUCLEASE: IDENTIFICATION OF THREE INTRAGENIC "GLOBAL" SUPPRESSORS OF NUCLEASE-MINUS MUTATIONS." Genetics 110, no. 4 (1985): 539–55. http://dx.doi.org/10.1093/genetics/110.4.539.

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ABSTRACT A collection of 77 unique missense mutations distributed across the gene encoding staphylococcal nuclease (nuc) has been assembled. These mutations were induced by random gap misrepair mutagenesis of the cloned gene and were identified in E. coli transformants expressing reduced levels of nuclease activity. Four nuc - mutations which alter amino acid residues at positions outside of the active site region of the enzyme were submitted to a second round of mutagenesis, and characterization of several independent NUC+ isolates lead to the identification of three second-site suppressor mu

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3

Herring, Christopher D., and Frederick R. Blattner. "Global Transcriptional Effects of a Suppressor tRNA and the Inactivation of the Regulator frmR." Journal of Bacteriology 186, no. 20 (2004): 6714–20. http://dx.doi.org/10.1128/jb.186.20.6714-6720.2004.

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ABSTRACT Expression of an amber suppressor tRNA should result in read-through of the 326 open reading frames (ORFs) that terminate with amber stop codons in the Escherichia coli genome, including six pseudogenes. Abnormal extension of an ORF might alter the activities of the protein and have effects on cellular physiology, while suppression of a pseudogene could lead to a gain of function. We used oligonucleotide microarrays to determine if any effects were apparent at the level of transcription in glucose minimal medium. Surprisingly, only eight genes had significantly different expression in

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4

Baroni, T. E., T. Wang, H. Qian, et al. "A global suppressor motif for p53 cancer mutants." Proceedings of the National Academy of Sciences 101, no. 14 (2004): 4930–35. http://dx.doi.org/10.1073/pnas.0401162101.

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5

Cheng, Chin Leng, Michael K. Wong, and Mark Hochstrasser. "Yeast Nst1 is a novel component of P-bodies and is a specific suppressor of proteasome base assembly defects." Molecular Biology of the Cell 32, no. 20 (2021): ar6. http://dx.doi.org/10.1091/mbc.e21-04-0178.

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We identified negative salt tolerance 1 (Nst1) as a dosage suppressor of the temperature sensitivity and proteasome assembly defects in multiple base mutants. Both endogenous and overexpressed Nst1 could localize to processing bodies. Nst1 overexpression inhibited global protein translation that in turn suppressed aggregation and proteasome assembly defects in base assembly mutants.

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6

Csink, A. K., R. Linsk, and J. A. Birchler. "Mosaic suppressor, a gene in Drosophila that modifies retrotransposon expression and interacts with zeste." Genetics 136, no. 2 (1994): 573–83. http://dx.doi.org/10.1093/genetics/136.2.573.

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Abstract A newly identified locus in Drosophila melanogaster, Mosaic suppressor (Msu), is described. This gene modifies the expression of white-apricot (wa), which is a copia retrotransposon-induced allele of the white gene. In addition to suppressing wa in a mosaic fashion, this mutation suppresses or enhances the expression of several other retrotransposon induced white alleles. Mutations in Msu alter copia transcript abundance and may regulate the expression of several other retrotransposons. While each of the two Msu isolates is homozygous lethal, heteroallelic escapers occur at a low freq

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7

Nahar, Rahul, Parham Ramezani-Rad, Sinisa Dovat, Maike Buchner, Thomas G. Graeber, and Markus Muschen. "Mechanisms of Ikaros-Mediated Tumor Suppression." Blood 118, no. 21 (2011): 408. http://dx.doi.org/10.1182/blood.v118.21.408.408.

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Abstract Abstract 408 Background: The Ikaros (IKZF1) tumor suppressor is deleted in >80% of the cases of Ph+ ALL. While Ikaros cooperates with pre-B cell receptor signaling to induce cell cycle exit in Ph+ ALL (Trageser et al., J Exp Med, 2009), the mechanism of Ikaros-mediated tumor suppression is poorly understood. Here we report on a series of genetic experiments that show that Ikaros (i) interferes with key survival pathways downstream of the BCR-ABL1 kinase, (ii) inhibits leukemia cell proliferation through interaction with the pre-B cell receptor signaling pathway and (iii) activates

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8

Irie, K., K. Yamaguchi, K. Kawase, and K. Matsumoto. "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." Molecular and Cellular Biology 14, no. 5 (1994): 3150–57. http://dx.doi.org/10.1128/mcb.14.5.3150-3157.1994.

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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, increase

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9

Irie, K., K. Yamaguchi, K. Kawase, and K. Matsumoto. "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." Molecular and Cellular Biology 14, no. 5 (1994): 3150–57. http://dx.doi.org/10.1128/mcb.14.5.3150.

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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, increase

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10

Huang, W., and T. Palzkill. "A natural polymorphism in -lactamase is a global suppressor." Proceedings of the National Academy of Sciences 94, no. 16 (1997): 8801–6. http://dx.doi.org/10.1073/pnas.94.16.8801.

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11

Ansseau, M., P. Papart, W. Pitchot, M. Timsit-Berthier, JJ Legros, and R. von Frenckell. "Dexamethasone suppression test and prediction of treatment response to selective antidepressants." European Psychiatry 7, no. 4 (1992): 191–94. http://dx.doi.org/10.1017/s0924933800005307.

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SummaryThe usefulness of the dexamethasone suppression test (DST) in the prediction of treatment response to selective antidepressants was tested in 56 major depressive inpatients. Following DST, patients were randomly assigned to treatment by either nomifensine, a catecholaminergic antidepressant, or zimeldine, a serotonergic antidepressant during a 3-week period and assessed by means of the second part of the Clinical Global Impressions (CGI-2). No significant difference was present between the 27 DST suppressor and the 29 DST non-suppressor patients in their overall clinical outcome. Moreov

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12

Wells, Derek H., and Sharon R. Long. "Mutations in rpoBC Suppress the Defects of a Sinorhizobium meliloti relA Mutant." Journal of Bacteriology 185, no. 18 (2003): 5602–10. http://dx.doi.org/10.1128/jb.185.18.5602-5610.2003.

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ABSTRACT The nitrogen-fixing symbiosis between Sinorhizobium meliloti and Medicago sativa requires complex physiological adaptation by both partners. One method by which bacteria coordinately control physiological adaptation is the stringent response, which is triggered by the presence of the nucleotide guanosine tetraphosphate (ppGpp). ppGpp, produced by the RelA enzyme, is thought to bind to and alter the ability of RNA polymerase (RNAP) to initiate and elongate transcription and affect the affinity of the core enzyme for various sigma factors. An S. meliloti relA mutant which cannot produce

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13

Augustus, Anne Marie, Teresa Celaya, Fasahath Husain, Matthew Humbard, and Rajeev Misra. "Antibiotic-Sensitive TolC Mutants and Their Suppressors." Journal of Bacteriology 186, no. 6 (2004): 1851–60. http://dx.doi.org/10.1128/jb.186.6.1851-1860.2004.

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ABSTRACT The TolC protein of Escherichia coli, through its interaction with AcrA and AcrB, is thought to form a continuous protein channel that expels inhibitors from the cell. Consequently, tolC null mutations display a hypersensitive phenotype. Here we report the isolation and characterization of tolC missense mutations that direct the synthesis of mutant TolC proteins partially disabled in their efflux role. All alterations, consisting of single amino acid substitutions, were localized within the periplasmic α-helical domain. In two mutants carrying an I106N or S350F substitution, the hyper

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14

Kaiser, Martin F., David C. Johnson, Ping Wu, et al. "Global methylation analysis identifies prognostically important epigenetically inactivated tumor suppressor genes in multiple myeloma." Blood 122, no. 2 (2013): 219–26. http://dx.doi.org/10.1182/blood-2013-03-487884.

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Key Points Epigenetic inactivation of tumor suppressor genes is associated with an unfavorable prognosis in multiple myeloma. Drug response and microenvironment interaction pathways are affected by epigenetic inactivation, linking tumor biology to prognosis.

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15

Krüger, Larissa, Christina Herzberg, Hermann Rath, et al. "Essentiality of c-di-AMP in Bacillus subtilis: Bypassing mutations converge in potassium and glutamate homeostasis." PLOS Genetics 17, no. 1 (2021): e1009092. http://dx.doi.org/10.1371/journal.pgen.1009092.

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In order to adjust to changing environmental conditions, bacteria use nucleotide second messengers to transduce external signals and translate them into a specific cellular response. Cyclic di-adenosine monophosphate (c-di-AMP) is the only known essential nucleotide second messenger. In addition to the well-established role of this second messenger in the control of potassium homeostasis, we observed that glutamate is as toxic as potassium for a c-di-AMP-free strain of the Gram-positive model bacterium Bacillus subtilis. In this work, we isolated suppressor mutants that allow growth of a c-di-

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16

Kinscherf, Thomas G., and David K. Willis. "Global Regulation by gidA in Pseudomonas syringae." Journal of Bacteriology 184, no. 8 (2002): 2281–86. http://dx.doi.org/10.1128/jb.184.8.2281-2286.2002.

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ABSTRACT Analysis of two virulence mutants of Pseudomonas syringae B728a revealed that the Tn 5 sites of insertion were within the gidA open reading frame (ORF). These mutations were pleiotropic, affecting diverse phenotypic traits, such as lipodepsipeptide (syringomycin and syringopeptin) antibiotic production, swarming, presence of fluorescent pigment, and virulence. Site-specific recombination of a disrupted gidA gene into the chromosome resulted in the same phenotypic pattern as transposon insertion. Mutant phenotypes were restored by the gidA ORF on a plasmid. The salA gene, a copy number

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17

Wang, Jen-Yeu, Altaf Hossain Sarker, Priscilla K. Cooper, and Michael R. Volkert. "The Single-Strand DNA Binding Activity of Human PC4 Prevents Mutagenesis and Killing by Oxidative DNA Damage." Molecular and Cellular Biology 24, no. 13 (2004): 6084–93. http://dx.doi.org/10.1128/mcb.24.13.6084-6093.2004.

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ABSTRACT Human positive cofactor 4 (PC4) is a transcriptional coactivator with a highly conserved single-strand DNA (ssDNA) binding domain of unknown function. We identified PC4 as a suppressor of the oxidative mutator phenotype of the Escherichia coli fpg mutY mutant and demonstrate that this suppression requires its ssDNA binding activity. Saccharomyces cerevisiae mutants lacking their PC4 ortholog Sub1 are sensitive to hydrogen peroxide and exhibit spontaneous and peroxide-induced hypermutability. PC4 expression suppresses the peroxide sensitivity of the yeast sub1Δ mutant, suggesting that

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18

Knights, Alexander J., Lu Yang, Manan Shah та ін. "Krüppel-like factor 3 (KLF3) suppresses NF-κB–driven inflammation in mice". Journal of Biological Chemistry 295, № 18 (2020): 6080–91. http://dx.doi.org/10.1074/jbc.ra120.013114.

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Bacterial products such as lipopolysaccharides (or endotoxin) cause systemic inflammation, resulting in a substantial global health burden. The onset, progression, and resolution of the inflammatory response to endotoxin are usually tightly controlled to avoid chronic inflammation. Members of the NF-κB family of transcription factors are key drivers of inflammation that activate sets of genes in response to inflammatory signals. Such responses are typically short-lived and can be suppressed by proteins that act post-translationally, such as the SOCS (suppressor of cytokine signaling) family. L

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19

Nagaraja, Ankur K., Chad J. Creighton, Zhifeng Yu, et al. "A Link between mir-100 and FRAP1/mTOR in Clear Cell Ovarian Cancer." Molecular Endocrinology 24, no. 2 (2010): 447–63. http://dx.doi.org/10.1210/me.2009-0295.

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Abstract MicroRNAs (miRNAs) are small noncoding RNAs that direct gene regulation through translational repression and degradation of complementary mRNA. Although miRNAs have been implicated as oncogenes and tumor suppressors in a variety of human cancers, functional roles for individual miRNAs have not been described in clear cell ovarian carcinoma, an aggressive and chemoresistant subtype of ovarian cancer. We performed deep sequencing to comprehensively profile miRNA expression in 10 human clear cell ovarian cancer cell lines compared with normal ovarian surface epithelial cultures and disco

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20

Trizzino, Marco, Elisa Barbieri, Ana Petracovici, et al. "The Tumor Suppressor ARID1A Controls Global Transcription via Pausing of RNA Polymerase II." Cell Reports 23, no. 13 (2018): 3933–45. http://dx.doi.org/10.1016/j.celrep.2018.05.097.

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21

Fan, Sijia, Jing Wang, Guangqing Yu, et al. "TET is targeted for proteasomal degradation by the PHD-pVHL pathway to reduce DNA hydroxymethylation." Journal of Biological Chemistry 295, no. 48 (2020): 16299–313. http://dx.doi.org/10.1074/jbc.ra120.014538.

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Hypoxia-inducible factors are heterodimeric transcription factors that play a crucial role in a cell's ability to adapt to low oxygen. The von Hippel-Lindau tumor suppressor (pVHL) acts as a master regulator of HIF activity, and its targeting of prolyl hydroxylated HIF-α for proteasomal degradation under normoxia is thought to be a major mechanism for pVHL tumor suppression and cellular response to oxygen. Whether pVHL regulates other targets through a similar mechanism is largely unknown. Here, we identify TET2/3 as novel targets of pVHL. pVHL induces proteasomal degradation of TET2/3, result

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Hajek, Michael, Asel Biktasova, Andrew Sewell, et al. "Global Genome Demethylation Causes Transcription-Associated DNA Double Strand Breaks in HPV-Associated Head and Neck Cancer Cells." Cancers 13, no. 1 (2020): 21. http://dx.doi.org/10.3390/cancers13010021.

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High levels of DNA methylation at CpG loci are associated with transcriptional repression of tumor suppressor genes and dysregulation of DNA repair genes. Human papilloma virus (HPV)-associated head and neck squamous cell carcinomas (HNSCC) have high levels of DNA methylation and methylation has been associated with dampening of an innate immune response in virally infected cells. We have been exploring demethylation as a potential treatment in HPV+ HNSCC and recently reported results of a window clinical trial showing that HNSCCs are particularly sensitive to demethylating agent 5-azacytidine

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Moreno-León, Carolina, and Francisco Aguayo. "Cooperation Between Aflatoxin-Induced p53 Aberrations and Hepatitis B Virus in Hepatocellular Carcinoma." Journal of Xenobiotics 15, no. 4 (2025): 96. https://doi.org/10.3390/jox15040096.

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Hepatocellular carcinoma (HCC) imposes a significant burden on global public health. Exposure to aflatoxins, potent mycotoxins produced by Aspergillus fungi contaminating staple foods, and chronic hepatitis B virus (HBV) infection are major etiological factors, especially where they co-exist. This review examines the critical role of the p53 tumor suppressor pathway as a primary target and convergence point for the carcinogenic actions of aflatoxins and HBV. Aflatoxin B1 (AFB1), a Group 1 carcinogen, exerts significant genotoxicity, characteristically inducing a specific hotspot mutation (R249

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Moggs, J. G., T. C. Murphy, F. L. Lim та ін. "Anti-proliferative effect of estrogen in breast cancer cells that re-express ERα is mediated by aberrant regulation of cell cycle genes". Journal of Molecular Endocrinology 34, № 2 (2005): 535–51. http://dx.doi.org/10.1677/jme.1.01677.

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Estrogen receptor (ER)-negative breast carcinomas do not respond to hormone therapy, making their effective treatment very difficult. The re-expression of ERα in ER-negative MDA-MB-231 breast cancer cells has been used as a model system, in which hormone-dependent responses can be restored. Paradoxically, in contrast to the mitogenic activity of 17β-estradiol (E2) in ER-positive breast cancer cells, E2 suppresses proliferation in ER-negative breast cancer cells in which ERα has been re-expressed. We have used global gene expression profiling to investigate the mechanism by which E2 suppresses

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25

Kucuk, Can, Xiaozhou Hu, Bei Jiang, et al. "Global Methylation Analysis Reveals Novel Candidate Tumor Suppressor Genes In Natural Killer Cell Lymphomas." Blood 122, no. 21 (2013): 1262. http://dx.doi.org/10.1182/blood.v122.21.1262.1262.

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Abstract Background Natural killer cell lymphomas (NKCLs) are aggressive neoplasms with poor prognosis. A few candidate tumor suppressor genes were identified with locus specific methylation analysis. However, no genome-wide study has been performed on NKCL cases to identify the spectrum of epigenetically silenced candidate genes contributing to the neoplastic transformation of NK cells. Methods Here, we analyzed genome-wide methylation profile in NKCL cases (n=12) and NK cell lines (n=2) by performing methyl-sensitive cut counting (MSCC). The methylation profile of malignant NK samples (n=14)

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Luense, Svenja, Philip Denner, Amaury Fernández-Montalván, et al. "Quantification of Histone H3 Lys27 Trimethylation (H3K27me3) by High-Throughput Microscopy Enables Cellular Large-Scale Screening for Small-Molecule EZH2 Inhibitors." Journal of Biomolecular Screening 20, no. 2 (2014): 190–201. http://dx.doi.org/10.1177/1087057114559668.

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EZH2 inhibition can decrease global histone H3 lysine 27 trimethylation (H3K27me3) and thereby reactivates silenced tumor suppressor genes. Inhibition of EZH2 is regarded as an option for therapeutic cancer intervention. To identify novel small-molecule (SMOL) inhibitors of EZH2 in drug discovery, trustworthy cellular assays amenable for phenotypic high-throughput screening (HTS) are crucial. We describe a reliable approach that quantifies changes in global levels of histone modification marks using high-content analysis (HCA). The approach was validated in different cell lines by using small

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Kanduri, Meena, Nicola Cahill, Hanna Göransson, et al. "Differential genome-wide array–based methylation profiles in prognostic subsets of chronic lymphocytic leukemia." Blood 115, no. 2 (2010): 296–305. http://dx.doi.org/10.1182/blood-2009-07-232868.

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Abstract Global hypomethylation and regional hypermethylation are well-known epigenetic features of cancer; however, in chronic lymphocytic leukemia (CLL), studies on genome-wide epigenetic modifications are limited. Here, we analyzed the global methylation profiles in CLL, by applying high-resolution methylation microarrays (27 578 CpG sites) to 23 CLL samples, belonging to the immunoglobulin heavy-chain variable (IGHV) mutated (favorable) and IGHV unmutated/IGHV3-21 (poor-prognostic) subsets. Overall, results demonstrated significant differences in methylation patterns between these subgroup

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Kobayashi, Hideki. "Inducible Suppression of Global Translation by Overuse of Rare Codons." Applied and Environmental Microbiology 81, no. 7 (2015): 2544–53. http://dx.doi.org/10.1128/aem.03708-14.

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ABSTRACTRecently, artificial gene networks have been developed in synthetic biology to control gene expression and make organisms as controllable as robots. Here, I present an artificial posttranslational gene-silencing system based on the codon usage bias and low tRNA content corresponding to minor codons. I engineered the green fluorescent protein (GFP) gene to inhibit translation indirectly with the lowest-usage codons to monopolize various minor tRNAs (lgfp). The expression oflgfpinterfered nonspecifically with the growth ofEscherichia coli,Saccharomyces cerevisiae, human HeLa cervical can

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Pramodh, Sreepoorna, Ritu Raina, Arif Hussain, et al. "Luteolin Causes 5′CpG Demethylation of the Promoters of TSGs and Modulates the Aberrant Histone Modifications, Restoring the Expression of TSGs in Human Cancer Cells." International Journal of Molecular Sciences 23, no. 7 (2022): 4067. http://dx.doi.org/10.3390/ijms23074067.

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Cancer progression is linked to abnormal epigenetic alterations such as DNA methylation and histone modifications. Since epigenetic alterations, unlike genetic changes, are heritable and reversible, they have been considered as interesting targets for cancer prevention and therapy by dietary compounds such as luteolin. In this study, epigenetic modulatory behaviour of luteolin was analysed on HeLa cells. Various assays including colony forming and migration assays, followed by biochemical assays of epigenetic enzymes including DNA methyltransferase, histone methyl transferase, histone acetyl t

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30

Küçük, Can, Xiaozhou Hu, Bei Jiang, et al. "Global Promoter Methylation Analysis Reveals Novel Candidate Tumor Suppressor Genes in Natural Killer Cell Lymphoma." Clinical Cancer Research 21, no. 7 (2015): 1699–711. http://dx.doi.org/10.1158/1078-0432.ccr-14-1216.

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Marciano, David C., Jeanine M. Pennington, Xiaohu Wang та ін. "Genetic and Structural Characterization of an L201P Global Suppressor Substitution in TEM-1 β-Lactamase". Journal of Molecular Biology 384, № 1 (2008): 151–64. http://dx.doi.org/10.1016/j.jmb.2008.09.009.

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Osorio-Pérez, Sofía Madeline, Carolina Estrada-Meza, Luis M. Ruiz-Manriquez, et al. "Thymoquinone Potentially Modulates the Expression of Key Onco- and Tumor Suppressor miRNAs in Prostate and Colon Cancer Cell Lines: Insights from PC3 and HCT-15 Cells." Genes 14, no. 9 (2023): 1730. http://dx.doi.org/10.3390/genes14091730.

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Prostate cancer (PC) and colon cancer significantly contribute to global cancer-related morbidity and mortality. Thymoquinone (TQ), a naturally occurring phytochemical found in black cumin, has shown potential as an anticancer compound. This study aimed to investigate the effects of TQ on the expression profile of key tumor suppressor and onco-suppressor miRNAs in PC3 prostate cancer cells and HCT-15 colon cancer cells. Cell viability assays revealed that TQ inhibited the growth of both cell lines in a dose-dependent manner, with IC50 values of approximately 82.59 μM for HCT-15 and 55.83 μM fo

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Iizuka, Masayoshi, Olga F. Sarmento, Takao Sekiya, Heidi Scrable, C. David Allis, and M. Mitchell Smith. "Hbo1 Links p53-Dependent Stress Signaling to DNA Replication Licensing." Molecular and Cellular Biology 28, no. 1 (2007): 140–53. http://dx.doi.org/10.1128/mcb.00662-07.

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ABSTRACT Hbo1 is a histone acetyltransferase (HAT) that is required for global histone H4 acetylation, steroid-dependent transcription, and chromatin loading of MCM2-7 during DNA replication licensing. It is the catalytic subunit of protein complexes that include ING and JADE proteins, growth regulatory factors and candidate tumor suppressors. These complexes are thought to act via tumor suppressor p53, but the molecular mechanisms and links between stress signaling and chromatin, are currently unknown. Here, we show that p53 physically interacts with Hbo1 and negatively regulates its HAT acti

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34

Chen, Y., and B. K. Tye. "The yeast Mcm1 protein is regulated posttranscriptionally by the flux of glycolysis." Molecular and Cellular Biology 15, no. 8 (1995): 4631–39. http://dx.doi.org/10.1128/mcb.15.8.4631.

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Mcm1 is a multifunctional protein which plays a role both in the initiation of DNA replication and in the transcriptional regulation of diverse genes in Saccharomyces cerevisiae. The mcm1-1 mutation results in instability of minichromosomes and alpha-specific sterility. Second-site suppressors that restore minichromosome stability but not fertility to the mcm1-1 mutant were isolated. Two of the suppressors, pgm1-1 and pgm1-2, are mutant alleles of PGM1 which encodes a glycolytic enzyme, phosphoglycerate mutase. We show that the pgm1-1 mutation suppresses the minichromosome maintenance (Mcm) de

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Ding, Yali, Bing He, Jonathon Payne, et al. "Regulation of Heterochromatin Landscape in T-Cell Acute Lymphoblastic Leukemia." Blood 138, Supplement 1 (2021): 2217. http://dx.doi.org/10.1182/blood-2021-154388.

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Abstract Ikzf1 encodes a zinc finger, DNA-binding protein that functions as a tumor suppressor in acute lymphoblastic leukemia (ALL). Deletion and/or loss of Ikaros function results in the development of high-risk leukemia. In the nucleus, Ikaros forms complexes with histone deacetylase complex, NuRD, and it participates in the formation of heterochromatin. The role of Ikaros-mediated formation of heterochromatin in tumor suppression in leukemia is unknown. We determined global genomic occupancy of Ikaros, global heterochromatin distribution, chromatin accessibility, DNA methylation landscape,

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Kawamata, Norihiko, Takayuki Saitoh, Sakura Sakajiri, and Phillip H. Koeffler. "Identification of Candidate Tumor Suppressor Genes Silenced Epigenetically in Mantle Cell Lymphoma." Blood 106, no. 11 (2005): 3001. http://dx.doi.org/10.1182/blood.v106.11.3001.3001.

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Abstract Many tumor suppressor genes are silenced by epigenetic mechanisms in human cancers, including mantle cell lymphoma (MCL). In this study, we have used a variety of research tools to screen for genes that are epigenetically silenced in MCL. Changes in the global gene expression profile of the MCL cell line, Jeko1, were analyzed after treatment with the combination of the demethylating agent, 5-aza-2′-deoxycytidine, and the histone deacetylase inhibitor, suberoyl anilide bishydroxamide, by DNA microarray technique. By screening over 22,000 genes, we identified 26 candidate tumor suppress

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Lycan, D., G. Mikesell, M. Bunger, and L. Breeden. "Differential effects of Cdc68 on cell cycle-regulated promoters in Saccharomyces cerevisiae." Molecular and Cellular Biology 14, no. 11 (1994): 7455–65. http://dx.doi.org/10.1128/mcb.14.11.7455-7465.1994.

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Swi4 and Swi6 form a complex which is required for Start-dependent activation of HO and for high-level expression of G1 cyclin genes CLN1 and CLN2. To identify other regulators of this pathway, we screened for dominant, recessive, conditional, and allele-specific suppressors of swi4 mutants. We isolated 16 recessive suppressors that define three genes, SSF1, SSF5, and SSF9 (suppressor of swi four). Mutations in all three genes bypass the requirement for both Swi4 and Swi6 for HO transcription and activate transcription from reporter genes lacking upstream activating sequences (UASs). SSF5 is a

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Lycan, D., G. Mikesell, M. Bunger, and L. Breeden. "Differential effects of Cdc68 on cell cycle-regulated promoters in Saccharomyces cerevisiae." Molecular and Cellular Biology 14, no. 11 (1994): 7455–65. http://dx.doi.org/10.1128/mcb.14.11.7455.

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Swi4 and Swi6 form a complex which is required for Start-dependent activation of HO and for high-level expression of G1 cyclin genes CLN1 and CLN2. To identify other regulators of this pathway, we screened for dominant, recessive, conditional, and allele-specific suppressors of swi4 mutants. We isolated 16 recessive suppressors that define three genes, SSF1, SSF5, and SSF9 (suppressor of swi four). Mutations in all three genes bypass the requirement for both Swi4 and Swi6 for HO transcription and activate transcription from reporter genes lacking upstream activating sequences (UASs). SSF5 is a

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Harford, Joe B. "A Second Career for p53 as A Broad-Spectrum Antiviral?" Viruses 15, no. 12 (2023): 2377. http://dx.doi.org/10.3390/v15122377.

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As the world exits the global pandemic caused by the previously unknown SARS-CoV-2, we also mark the 30th anniversary of p53 being named “molecule of the year” by Science based on its role as a tumor suppressor. Although p53 was originally discovered in association with a viral protein, studies on its role in preventing carcinogenesis have far overshadowed research related to p53′s role in viral infections. Nonetheless, there is an extensive body of scientific literature demonstrating that p53 is a critical component of host immune responses to viral infections. It is striking that diverse vir

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Seong, Rak-Kyun, Jae Kyung Lee, and Ok Sarah Shin. "Zika Virus-Induction of the Suppressor of Cytokine Signaling 1/3 Contributes to the Modulation of Viral Replication." Pathogens 9, no. 3 (2020): 163. http://dx.doi.org/10.3390/pathogens9030163.

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Zika virus (ZIKV) is a mosquito-borne flavivirus that has emerged and caused global outbreaks since 2007. Although ZIKV proteins have been shown to suppress early anti-viral innate immune responses, little is known about the exact mechanisms. This study demonstrates that infection with either the African or Asian lineage of ZIKV leads to a modulated expression of suppressor of cytokine signaling (SOCS) genes encoding SOCS1 and SOCS3 in the following cell models: A549 human lung adenocarcinoma cells; JAr human choriocarcinoma cells; human neural progenitor cells. Studies of viral gene expressio

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Rodrigue, Amélie, Guillaume Margaillan, Thiago Torres Gomes, et al. "A global functional analysis of missense mutations reveals two major hotspots in the PALB2 tumor suppressor." Nucleic Acids Research 47, no. 20 (2019): 10662–77. http://dx.doi.org/10.1093/nar/gkz780.

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Abstract While biallelic mutations in the PALB2 tumor suppressor cause Fanconi anemia subtype FA-N, monoallelic mutations predispose to breast and familial pancreatic cancer. Although hundreds of missense variants in PALB2 have been identified in patients to date, only a few have clear functional and clinical relevance. Herein, we investigate the effects of 44 PALB2 variants of uncertain significance found in breast cancer patients and provide detailed analysis by systematic functional assays. Our comprehensive functional analysis reveals two hotspots for potentially deleterious variations wit

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Scholl, Amanda, Alexander Muselman, and Dong-Er Zhang. "An Intronic Suppressor Element Regulates RUNX1 Alternative Polyadenylation." Blood 126, no. 23 (2015): 3578. http://dx.doi.org/10.1182/blood.v126.23.3578.3578.

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Abstract Polyadenylation is a post-transcriptional modification where the 3' end of an mRNA is cleaved and 250-300 adenines are added. It is predicted that 70-75% of human genes have more than one polyadenylation sequence (PAS) and are subject to alternative polyadenylation (APA). APA events affect the coding sequence of a gene when a proximal PAS is located within an intron, constitutive exon, or alternative exon. Gene expression is also affected if there are multiple PAS within the distal 3' untranslated region (UTR); proximal PAS usage shortens the 3'UTR, which can remove cis-regulatory reg

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Kampa, Kerstin M., Sandra Mueller, Michael Bonin, Marcus M. Schittenhelm, and Charles D. Lopez. "Insights Into the Role of ASPP2 (Apoptosis Stimulating Protein of p53-2) in Lymphomagenesis." Blood 114, no. 22 (2009): 1967. http://dx.doi.org/10.1182/blood.v114.22.1967.1967.

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Abstract Abstract 1967 Poster Board I-990 ASPP2 is a member of a family of p53 binding proteins that enhance apoptosis, in part through selective stimulation of p53 transactivation of pro-apoptotic target genes. Low ASPP2 expression is found in many human cancers and has been associated with poor clinical outcome in patients with aggressive lymphoma. Using an ASPP2+/- mouse model, we have previously demonstrated that ASPP2 is a haploinsufficient tumor suppressor and that reduced ASPP2 expression results in attenuated damage-response thresholds (Kampa et al., PNAS 2009). While ASPP2-/- mice are

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Crang, Nick, Khushboo Borah, Euan K. James, et al. "Role and Regulation of Poly-3-Hydroxybutyrate in Nitrogen Fixation in Azorhizobium caulinodans." Molecular Plant-Microbe Interactions® 34, no. 12 (2021): 1390–98. http://dx.doi.org/10.1094/mpmi-06-21-0138-r.

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An Azorhizobium caulinodans phaC mutant (OPS0865) unable to make poly-3-hydroxybutyrate (PHB), grows poorly on many carbon sources and cannot fix nitrogen in laboratory culture. However, when inoculated onto its host plant, Sesbania rostrata, the phaC mutant consistently fixed nitrogen. Upon reisolation from S. rostrata root nodules, a suppressor strain (OPS0921) was isolated that has significantly improved growth on a variety of carbon sources and also fixes nitrogen in laboratory culture. The suppressor retains the original mutation and is unable to synthesize PHB. Genome sequencing revealed

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Capuozzo, Maurizio, Mariachiara Santorsola, Marco Bocchetti, et al. "p53: From Fundamental Biology to Clinical Applications in Cancer." Biology 11, no. 9 (2022): 1325. http://dx.doi.org/10.3390/biology11091325.

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p53 tumour suppressor gene is our major barrier against neoplastic transformation. It is involved in many cellular functions, including cell cycle arrest, senescence, DNA repair, apoptosis, autophagy, cell metabolism, ferroptosis, immune system regulation, generation of reactive oxygen species, mitochondrial function, global regulation of gene expression, miRNAs, etc. Its crucial importance is denounced by the high percentage of amino acid sequence identity between very different species (Homo sapiens, Drosophila melanogaster, Rattus norvegicus, Danio rerio, Canis lupus familiaris, Gekko japon

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Menghi, Francesca, Koichiro Inaki, XingYi Woo, et al. "The tandem duplicator phenotype as a distinct genomic configuration in cancer." Proceedings of the National Academy of Sciences 113, no. 17 (2016): E2373—E2382. http://dx.doi.org/10.1073/pnas.1520010113.

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Next-generation sequencing studies have revealed genome-wide structural variation patterns in cancer, such as chromothripsis and chromoplexy, that do not engage a single discernable driver mutation, and whose clinical relevance is unclear. We devised a robust genomic metric able to identify cancers with a chromotype called tandem duplicator phenotype (TDP) characterized by frequent and distributed tandem duplications (TDs). Enriched only in triple-negative breast cancer (TNBC) and in ovarian, endometrial, and liver cancers, TDP tumors conjointly exhibit tumor protein p53 (TP53) mutations, disr

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McCoy, James M., Rebecca J. Stewart, Alessandro D. Uboldi, et al. "A forward genetic screen identifies a negative regulator of rapid Ca2+-dependent cell egress (MS1) in the intracellular parasite Toxoplasma gondii." Journal of Biological Chemistry 292, no. 18 (2017): 7662–74. http://dx.doi.org/10.1074/jbc.m117.775114.

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Toxoplasma gondii, like all apicomplexan parasites, uses Ca2+ signaling pathways to activate gliding motility to power tissue dissemination and host cell invasion and egress. A group of “plant-like” Ca2+-dependent protein kinases (CDPKs) transduces cytosolic Ca2+ flux into enzymatic activity, but how they function is poorly understood. To investigate how Ca2+ signaling activates egress through CDPKs, we performed a forward genetic screen to isolate gain-of-function mutants from an egress-deficient cdpk3 knockout strain. We recovered mutants that regained the ability to egress from host cells t

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Li, Wei, and Chung-Dar Lu. "Regulation of Carbon and Nitrogen Utilization by CbrAB and NtrBC Two-Component Systems in Pseudomonas aeruginosa." Journal of Bacteriology 189, no. 15 (2007): 5413–20. http://dx.doi.org/10.1128/jb.00432-07.

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ABSTRACT The global effect of the CbrAB and NtrBC two-component systems on the control of carbon and nitrogen utilization in Pseudomonas aeruginosa was characterized by phenotype microarray analyses with single and double mutants and the isogenic parent strain. The tested compounds were clustered based on the growth phenotypes of these strains, and the results clearly demonstrated the pivotal roles of CbrAB and NtrBC in carbon and nitrogen utilization, respectively. Growth of the cbrAB deletion mutant on arginine, histidine, and polyamines used as the sole carbon source was abolished, while gr

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Ergun, Pelin, Tina L. Samuels, Angela J. Mathison, et al. "Global Transcriptomic Analysis of Topical Sodium Alginate Protection against Peptic Damage in an In Vitro Model of Treatment-Resistant Gastroesophageal Reflux Disease." International Journal of Molecular Sciences 25, no. 19 (2024): 10714. http://dx.doi.org/10.3390/ijms251910714.

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Breakthrough symptoms are thought to occur in roughly half of all gastroesophageal reflux disease (GERD) patients despite maximal acid suppression (proton pump inhibitor, PPI) therapy. Topical alginates have recently been shown to enhance mucosal defense against acid-pepsin insult during GERD. We aimed to examine potential alginate protection of transcriptomic changes in a cell culture model of PPI-recalcitrant GERD. Immortalized normal-derived human esophageal epithelial cells underwent pretreatment with commercial alginate-based anti-reflux medications (Gaviscon Advance or Gaviscon Double Ac

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Burgon, Trever B., Jomaquai A. Jenkins, Stephen B. Deitz, Jeannie F. Spagnolo, and Karla Kirkegaard. "Bypass Suppression of Small-Plaque Phenotypes by a Mutation in Poliovirus 2A That Enhances Apoptosis." Journal of Virology 83, no. 19 (2009): 10129–39. http://dx.doi.org/10.1128/jvi.00642-09.

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ABSTRACT The rate of protein secretion in host cells is inhibited during infection with several different picornaviruses, with consequences likely to have significant effects on viral growth, spread, and pathogenesis. This Sin + (secretion inhibition) phenotype has been documented for poliovirus, foot-and-mouth disease virus, and coxsackievirus B3 and can lead to reduced cell surface expression of major histocompatibility complex class I and tumor necrosis factor receptor as well as reduced extracellular secretion of induced cytokines such as interleukin-6 (IL-6), IL-8, and beta interferon. Th

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