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Journal articles on the topic 'Gene H'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Schejbel, L., I. M. Schmidt, M. Kirchhoff, C. B. Andersen, H. V. Marquart, P. Zipfel, and P. Garred. "Complement factor H deficiency and endocapillary glomerulonephritis due to paternal isodisomy and a novel factor H mutation." Genes & Immunity 12, no. 2 (January 27, 2011): 90–99. http://dx.doi.org/10.1038/gene.2010.63.

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2

Brenner, Steven E., Tim Hubbard, Alexey Murzin, and Cyrus Chothia. "Gene duplications in H. influenzae." Nature 378, no. 6553 (November 1995): 140. http://dx.doi.org/10.1038/378140a0.

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3

Trefethen, Lloyd N. "Gene H. Golub (1932–2007)." Nature 450, no. 7172 (December 2007): 962. http://dx.doi.org/10.1038/450962a.

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4

Dale, J. B., and A. L. Bisno. "In Memoriam: Gene H. Stollerman." Clinical Infectious Diseases 59, no. 12 (September 8, 2014): 1805–6. http://dx.doi.org/10.1093/cid/ciu718.

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5

Thomasma, David C. "Laudation: Gene H. Stollerman, MD." Journal of the American Geriatrics Society 37, no. 1 (January 1989): 75. http://dx.doi.org/10.1111/j.1532-5415.1989.tb01572.x.

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6

Meurant, Gérard. "Gene H. Golub 1932–2007." Numerical Algorithms 51, no. 1 (November 7, 2008): 1–4. http://dx.doi.org/10.1007/s11075-008-9245-0.

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7

Simpson, Elizabeth, Phillip Chandler, Anne McLaren, Els Goulmy, Christine M. Disteche, David C. Page, and Malcolm A. Ferguson-Smith. "Mapping the H-Y gene." Development 101, Supplement (March 1, 1987): 157–61. http://dx.doi.org/10.1242/dev.101.supplement.157.

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This paper uses cytotoxic and proliferative T cell clones specific for H-Y and restricted by MHC molecules to type mice and humans inheriting incomplete portions of the Y chromosome. The data have allowed us to map the H-Y antigen gene Hya in mouse to a position closely linked with, but separable from, Tdy on the Sxr fragment and thus presumably to a position of the normal mouse Y chromosome near the centromere. The human H-Y gene maps between deletion intervals 4B and 7, separate from TDF which is on interval 1. We are currently testing cells from a number of additional patients who have inherited different portions of the Y chromosome to pinpoint the mapping more closely. It is of interest that in mouse a Y-linked gene controlling spermatogenesis (Spy) maps near Hya on the Sxr fragment: they could be the same or closely linked genes. In man, a gene controlling spermatogenesis maps to Yq and the data so far do not exclude that it could be coincident with the H-Y gene.

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8

Wolf, Konrad, Widmar Tanner, and Norbert Sauer. "The Chlorella H+/hexose cotransporter gene." Current Genetics 19, no. 3 (March 1991): 215–19. http://dx.doi.org/10.1007/bf00336489.

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9

Ishidoh, Kazumi, Eiki Kominami, Nobuhiko Katunuma, and Koichi Suzuki. "Gene structure of rat cathepsin H." FEBS Letters 253, no. 1-2 (August 14, 1989): 103–7. http://dx.doi.org/10.1016/0014-5793(89)80939-1.

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10

Caruthers, Marvin H. "Gene synthesis with H G Khorana." Resonance 17, no. 12 (December 2012): 1143–56. http://dx.doi.org/10.1007/s12045-012-0131-7.

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11

Shi, Jian, Rongfeng Liu, Guanglei Huang, Lixing Wang, Baoen Shan, Ningning Luo, Qin Zhang, Yaqing Wu, Yingxue Qi, and Chuang Qi. "SYK gene mutations with TMB-H and MSI-H in solid tumors." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e14572-e14572. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e14572.

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e14572 Background: Spleen tyrosine kinase ( SYK) gene encodes a cytoplasmic non-receptor tyrosine kinase (NRTK) and mediates signal transduction downstream of multiple transmembrane receptors, which plays an important role in a variety of signaling pathways. The change of SYK gene expression and gene mutations may lead to the formation and metastasis of multiple solid tumors. Previous studies on SYK mostly focus on the protein isomers and the methylation of SYK gene promoter. We previously used next generation sequencing (NGS) to explore SYK gene mutations on DNA level and found novel mutation types of SYK gene. Herein, NGS were performed to explore the relationship of SYK gene mutations with TMB and MSI in solid tumors for further clinical research. Methods: We retrospectively collected NGS detection data by 539-gene panel in 5648 patients with pan-cancer, of which 3931 patients by tumor tissue and 1717 patients by blood ctDNA, and screened out somatic SYK gene mutations. 539-gene panel contained all exon regions of SYK gene. Then we divided 5648 patients into four groups depending on whether SYK gene mutations: tumor tissue mutant group (T-mut) / non-mutant group (T-non-mut), and ctDNA mutant group (ctDNA-mut) / non-mutant group (ctDNA-non-mut). The difference in TMB between T-mut and T-non-mut groups; between ctDNA-mut and ctDNA-non-mut groups were analyzed via the Wilcoxon sign test respectively. The difference in MSI between T-mut and T-non-mut groups were analyzed via Fisher test. Results: In 5648 patients with solid tumors, 64 patients (48/3931 in tumor tissue and 16/1717 in blood ctDNA) were found harboring SYK gene mutations and the mutation frequency was 1.13%. TMB in T-mut group was higher than in T-non-mut group and significant difference of TMB was found via the Wilcoxon sign test (p = 5.3e-12) between the two groups. TMB in ctDNA-mut group was higher than in ctDNA-non-mut group and significant difference of TMB was found too (p = 4.6e-05). 12 patients were found MSI-H in T-mut group (12/48) and 53 patients were found MSI-H in T-non-mut group (35/3875). We found significant difference in the probability of MSI-H occurrence between the two groups by Fisher test (p = 6.531e-12, HR: 23.933, 95%CI: 10.734-50.415). Conclusions: This is the first report on the relationship between SYK gene mutations with TMB and MSI in solid tumors and we found that SYK gene mutations are associated with TMB-H and MSI-H in solid tumors. As a retrospective study in solid tumors, the conclusion and the mechanism need to be studied in the future.

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12

Mao, Steve. "Phase separation and gene control." Science 361, no. 6400 (July 26, 2018): 375.8–377. http://dx.doi.org/10.1126/science.361.6400.375-h.

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13

Yang, Weidong, Huayan Wang, and Larry Fliegel. "Regulation of Na+/H+Exchanger Gene Expression." Journal of Biological Chemistry 271, no. 34 (August 23, 1996): 20444–49. http://dx.doi.org/10.1074/jbc.271.34.20444.

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14

de Antonellis, Pasqualino. "Hepatocellular carcinoma: H-Prune gene regulatory networks." EBioMedicine 41 (March 2019): 21–22. http://dx.doi.org/10.1016/j.ebiom.2019.02.007.

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15

David, Véronique, Panos Papadopoulos, Jacqueline Yaouanq, Martine Blayau, Laurent Abel, Elizabetta Zappone, Muriel Perichon, Jim Drysdale, Jean-Yves Le Gall, and Marcel Simon. "Ferritin H gene polymorphism in idiopathic hemochromatosis." Human Genetics 81, no. 2 (January 1989): 123–26. http://dx.doi.org/10.1007/bf00293887.

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16

MISIANO, G. "Expression of H-related gene products in a factor H deficient family." Molecular Immunology 30 (September 1993): 33. http://dx.doi.org/10.1016/0161-5890(93)90291-i.

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17

Xing, C., T. A. Sivakumaran, J. J. Wang, E. Rochtchina, T. Joshi, W. Smith, P. Mitchell, and S. K. Iyengar. "Complement factor H polymorphisms, renal phenotypes and age-related macular degeneration: the Blue Mountains Eye Study." Genes & Immunity 9, no. 3 (March 13, 2008): 231–39. http://dx.doi.org/10.1038/gene.2008.10.

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18

Clauset, Aaron. "Assessing U.S. support for gene drives." Science 365, no. 6458 (September 12, 2019): 1131.8–1132. http://dx.doi.org/10.1126/science.365.6458.1131-h.

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19

Ovrutska, I. I., and D. A. Bluma. "Water deficit induces changes in H+-ATPase activity and its gene expression inZea maysL. roots." Reports of the National Academy of Sciences of Ukraine, no. 10 (November 16, 2016): 84–87. http://dx.doi.org/10.15407/dopovidi2016.10.084.

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20

VANDEGUCHTE, M., J. KOK, and G. VENEMA. "Gene expression in." FEMS Microbiology Letters 88, no. 2 (February 1992): 73–92. http://dx.doi.org/10.1016/0378-1097(92)90685-h.

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21

Kelner, Katrina L. "Improving gene editing in human T cells." Science 350, no. 6256 (October 1, 2015): 52.8–53. http://dx.doi.org/10.1126/science.350.6256.52-h.

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22

MATSUSHIMA, M., A. TODISCO, N. ZOUBI, and C. DICKINSON. "Gastria regulation of H+−K+-ATPase gene expression." Gastroenterology 120, no. 5 (April 2001): A9. http://dx.doi.org/10.1016/s0016-5085(01)80045-7.

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23

Matsushima, Masashi, Andrea Todisco, Najeed Zoubi, and Chris J. Dickinson. "Gastria regulation of H+−K+-ATPase gene expression." Gastroenterology 120, no. 5 (April 2001): A9. http://dx.doi.org/10.1016/s0016-5085(08)80045-5.

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24

Vik, D. P., J. B. Keeney, P. Muñoz-Cánoves, D. D. Chaplin, and B. F. Tack. "Structure of the murine complement factor H gene." Journal of Biological Chemistry 263, no. 32 (November 1988): 16720–24. http://dx.doi.org/10.1016/s0021-9258(18)37450-7.

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25

Tsuji, Yoshiaki, Elizabeth Moran, Suzy V. Torti, and Frank M. Torti. "Transcriptional Regulation of the Mouse Ferritin H Gene." Journal of Biological Chemistry 274, no. 11 (March 12, 1999): 7501–7. http://dx.doi.org/10.1074/jbc.274.11.7501.

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26

Chisholm, Edward James. "R024: Nanoparticle H&N Cancer Gene Therapy." Otolaryngology–Head and Neck Surgery 137, no. 2_suppl (August 2007): P157. http://dx.doi.org/10.1016/j.otohns.2007.06.358.

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27

Koyata, Hirohisa, and Koichi Hiraga. "Partial structure of the human H-protein gene." Biochemical and Biophysical Research Communications 178, no. 3 (August 1991): 1072–77. http://dx.doi.org/10.1016/0006-291x(91)91001-s.

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28

Chaurasiya, Kathy R., Ramon van der Valk, Bram Henneman, and Remus T. Dame. "Vizualizing the Mechanism of H-NS Gene Regulation." Biophysical Journal 114, no. 3 (February 2018): 439a. http://dx.doi.org/10.1016/j.bpj.2017.11.2430.

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29

Read, Timothy D., Sarah W. Satola, Jason A. Opdyke, and Monica M. Farley. "Copy Number of Pilus Gene Clusters inHaemophilus influenzae and Variation in the hifEPilin Gene." Infection and Immunity 66, no. 4 (April 1, 1998): 1622–31. http://dx.doi.org/10.1128/iai.66.4.1622-1631.1998.

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ABSTRACT Brazilian purpuric fever (BPF)-associated Haemophilus influenzae biogroup aegyptius strain F3031 contains two identical copies of a five gene cluster (hifA to hifE) encoding pili similar to well-characterized Hif fimbriae of H. influenzae type b. HifE, the putative pilus tip adhesin of F3031, shares only 40% amino acid sequence similarity with the same molecule from type b strains, whereas the other four proteins have 75 to 95% identity. To determine whether pilus cluster duplication and thehifE F3031 allele were special features of BPF-associated bacteria, we analyzed a collection of H. influenzae strains by PCR with hifA- andhifE-specific oligonucleotides, by Southern hybridization with a hifC gene probe, and by nucleotide sequencing. The presence of two pilus clusters was limited to some H. influenzae biogroup aegyptius strains. ThehifE F3031 allele was limited to H. influenzae biogroup aegyptius. Two strains contained one copy ofhifE F3031 and one copy of a varianthifE allele. We determined the nucleotide sequences of fourhifE genes from H. influenzae biogroup aegyptius and H. influenzae capsule serotypes a and c. The predicted proteins produced by these genes demonstrated only 35 to 70% identity to the three published HifE proteins from nontypeable H. influenzae, serotype b, and BPF strains. The C-terminal third of the molecules implicated in chaperone binding was the most highly conserved region. Three conserved domains in the otherwise highly variable N-terminal putative receptor-binding region of HifE were similar to conserved portions in the N terminus ofNeisseria pilus adhesin PilC. We concluded that two pilus clusters and hifE F3031 were not specific for BPF-causing H. influenzae, and we also identified portions of HifE possibly involved in binding mammalian cell receptors.

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30

Martin, Kimberly, Gregory Morlin, Arnold Smith, Andrea Nordyke, Abraham Eisenstark, and Miriam Golomb. "The Tryptophanase Gene Cluster of Haemophilus influenzae Type b: Evidence for Horizontal Gene Transfer." Journal of Bacteriology 180, no. 1 (January 1, 1998): 107–18. http://dx.doi.org/10.1128/jb.180.1.107-118.1998.

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ABSTRACT Among strains of Haemophilus influenzae, the ability to catabolize tryptophan (as detected by indole production) varies and is correlated with pathogenicity. Tryptophan catabolism is widespread (70 to 75%) among harmless respiratory isolates but is nearly universal (94 to 100%) among strains causing serious disease, including meningitis. As a first step in investigating the relationship between tryptophan catabolism and virulence, we have identified genes in pathogenic H. influenzae which are homologous to the tryptophanase (tna) operon of Escherichia coli. The tna genes are located on a 3.1-kb fragment betweennlpD and mutS in the H. influenzaetype b (Eagan) genome, are flanked by 43-bp direct repeats of an uptake signal sequence downstream from nlpD, and appear to have been inserted as a mobile unit within this sequence. The organization of this insertion is reminiscent of pathogenicity islands. Thetna cluster is found at the same map location in all indole-positive strains of H. influenzae surveyed and is absent from reference type d and e genomes. In contrast to H. influenzae, most other Haemophilus species lacktna genes. Phylogenetic comparisons suggest that thetna cluster was acquired by intergeneric lateral transfer, either by H. influenzae or a recent ancestor, and thatE. coli may have acquired its tnaA gene from a related source. Genomes of virulent H. influenzae resemble those of pathogenic enterics in having an island of laterally transferred DNA next to mutS.

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31

Palmgren, Michael Gjedde, and Gertrud Christensen. "Complementation in situ of the yeast plasma membrane H+ -ATPase gene pmal by an H+ -ATPase gene from a heterologous species." FEBS Letters 317, no. 3 (February 15, 1993): 216–22. http://dx.doi.org/10.1016/0014-5793(93)81279-9.

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32

Azoulay-Cayla, Arièle, Sylvie Syan, Michel Brahic, and Jean-François Bureau. "Roles of the H-2D b and H-K b genes in resistance to persistent Theiler’s murine encephalomyelitis virus infection of the central nervous system." Journal of General Virology 82, no. 5 (May 1, 2001): 1043–47. http://dx.doi.org/10.1099/0022-1317-82-5-1043.

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Theiler’s murine encephalomyelitis virus, a member of the Picornaviridae family, persists in the spinal cord of susceptible strains of mice. Resistant strains of mice, such as the H-2 b strain, clear the virus infection after an acute encephalomyelitis. The H-2D locus, but not the H-2K locus, has a major effect on this resistance, although both loci code for MHC class I molecules with similar general properties. For the present work, we rendered susceptible H-2 q FVB/N mice transgenic for either the H-2D b gene, the H-2K b gene or a chimeric H-2D b /K b gene in which the exons encoding the peptide-binding groove of the H-2K b gene have been replaced by those of the H-2D b gene. Mice transgenic for either the H-2D b gene or the chimeric H-2D b /K b gene were significantly more resistant to persistent virus infection than mice transgenic for the H-2K b gene, suggesting that the difference in the effects of the H-2D b gene and the H-2K b gene are due to the nature of the peptides presented by these class I molecules.

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33

Morahan, Grant, and Steven Rakar. "Localization of the Mouse Na+/H+ Exchanger Gene on Distal Chromosome 4." Genomics 15, no. 1 (January 1993): 231–32. http://dx.doi.org/10.1006/geno.1993.1044.

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34

Katae, Masaharu, Yasushi Miyahira, Kazuyoshi Takeda, Hironori Matsuda, Hideo Yagita, Ko Okumura, Tsutomu Takeuchi, et al. "Coadministration of an Interleukin-12 Gene and a Trypanosoma cruzi Gene Improves Vaccine Efficacy." Infection and Immunity 70, no. 9 (September 2002): 4833–40. http://dx.doi.org/10.1128/iai.70.9.4833-4840.2002.

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ABSTRACT We tested the immunogenicity of two Trypanosoma cruzi antigens injected into mice in the form of DNA vaccine. Immunization with DNA encoding dihydroorotate dehydrogenase did not confer protective immunity in all mouse strains tested. Immunization with DNA encoding trans-sialidase surface antigen (TSSA) protected C57BL/6 (H-2b ) mice but not BALB/c (H-2d ) or C3H/Hej (H-2k ) mice against lethal T. cruzi infection. In vivo depletion of CD4+ or CD8+ T cells abolished the protective immunity elicited by TSSA gene in C57BL/6 mice. Enzyme-linked immunospot assay with splenocytes from T. cruzi-infected mice or TSSA gene-vaccinated mice identified an H-2Kb -restricted antigenic peptide, ANYNFTLV. The CD8+-T-cell line specific for this peptide could recognize T. cruzi-infected cells in vitro and could protect naive mice from lethal infection when adoptively transferred. Coadministration of the interleukin-12 (IL-12) gene with the TSSA gene facilitated the induction of ANYNFTLV-specific CD8+ T cells and improved the vaccine efficacy against lethal T. cruzi infection. These results reinforced the utility of immunomodulatory adjuvants such as IL-12 gene for eliciting protective immunity against intracellular parasites by DNA vaccination.

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35

Milasin, J., N. Pujić, N. Dedović, M. Gavrić, V. Vranić, V. Petrović, and A. Minić. "H-ras gene mutations in salivary gland pleomorphic adenomas." International Journal of Oral and Maxillofacial Surgery 22, no. 6 (December 1993): 359–61. http://dx.doi.org/10.1016/s0901-5027(05)80668-x.

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36

Viquez, Olga M., Koffi N. Konan, and Hortense W. Dodo. "Genomic organization of peanut allergen gene, Ara h 3." Molecular Immunology 41, no. 12 (November 2004): 1235–40. http://dx.doi.org/10.1016/j.molimm.2004.06.033.

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37

SCHONDORF, T., A. ANDRACK, D. NIEDERACHER, M. BECKER, H. ENGEL, A. SCHARL, and U. GOHRING. "The H-ras gene in primary human breast cancer." Journal of the Society for Gynecologic Investigation 5, no. 1 (January 1998): 84A. http://dx.doi.org/10.1016/s1071-5576(97)86256-9.

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38

Stratton, M. R., C. J. Marshall, C. S. Cooper, Abhijit Nag, JeffreyA Jones, RoyG Smith, PatA Wright, NickR Lemoine, E. Dilwyn Williams, and David Wynford-Thomas. "ALTERED c-H-ras GENE IN NON-NEOPLASTIC TISSUE." Lancet 333, no. 8639 (March 1989): 668–69. http://dx.doi.org/10.1016/s0140-6736(89)92169-7.

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39

Xu, J., P. B. Dallas, P. A. Lyons, G. R. Shellam, and A. A. Scalzo. "Identification of the glycoprotein H gene of murine cytomegalovirus." Journal of General Virology 73, no. 7 (July 1, 1992): 1849–54. http://dx.doi.org/10.1099/0022-1317-73-7-1849.

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40

Nelson, Kristie L., Nicole A. Becker, Gurcharan S. Pahwa, Michael A. Hollingsworth, and L. James Maher. "Potential for H-DNA in the HumanMUC1Mucin Gene Promoter." Journal of Biological Chemistry 271, no. 30 (July 26, 1996): 18061–67. http://dx.doi.org/10.1074/jbc.271.30.18061.

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41

Choudhury, Noura, Sicheng Wen, Victoria E. Ruiz, Songhua Zhang, Jason T. Machan, and Steven F. Moss. "Gastrokine Gene Expression During H. pylori Infection in Mice." Gastroenterology 140, no. 5 (May 2011): S—469. http://dx.doi.org/10.1016/s0016-5085(11)61931-8.

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42

Yachou, Abdel-kader, Françoise Renaudie, Bernard Grandchamp, and Carole Beaumont. "Nucleotide sequence of the mouse ferritin H chain gene." Nucleic Acids Research 17, no. 19 (1989): 8005. http://dx.doi.org/10.1093/nar/17.19.8005.

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43

Nishioka, Yoshihiro, Kanji Kobayashi, Satoru Sagae, Masaki Sugimura, Shinichi Ishioka, Masami Nagata, Katuhiko Terasawa, Takashi Tokino, and Ryuichi Kudo. "Mutational Analysis of STK11 h Gene in Ovarian Carcinomas." Japanese Journal of Cancer Research 90, no. 6 (June 1999): 629–32. http://dx.doi.org/10.1111/j.1349-7006.1999.tb00793.x.

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44

Totaro, A., A. Grifa, M. Carella, L. D'Ambrosio, M. Valentino, M. P. Roth, N. Borot, et al. "Hereditary hemochromatosis: aHpal polymorphism within the HLA-H gene." Molecular and Cellular Probes 11, no. 3 (June 1997): 229–30. http://dx.doi.org/10.1006/mcpr.1997.0102.

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45

Yoo, Jinyoung, and Robert A. Robinson. "H-ras gene mutations in salivary gland mucoepidermoid carcinomas." Cancer 88, no. 3 (February 1, 2000): 518–23. http://dx.doi.org/10.1002/(sici)1097-0142(20000201)88:3<518::aid-cncr4>3.0.co;2-w.

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46

Cai, Zeling, and LarryR Pease. "An intragenic recombinant class I gene: H-2D dx." Immunogenetics 34, no. 4 (October 1991): 273–76. http://dx.doi.org/10.1007/bf00215266.

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47

Pribyl, T. M., and H. G. Martinson. "Transcription termination at the chicken beta H-globin gene." Molecular and Cellular Biology 8, no. 12 (December 1988): 5369–77. http://dx.doi.org/10.1128/mcb.8.12.5369.

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We characterized the transcription termination region of the chicken beta H-globin gene. First we located the region by nuclear runon transcription in vitro. Then we sequenced and subcloned it into a chloramphenicol acetyltransferase (CAT) expression vector for assay in vivo. The region of beta H termination contains two interesting elements located about 1 kilobase downstream of the beta H gene poly(A) site. Either element alone can block CAT expression if inserted between the promoter and the poly(A) site of the cat gene in pRSVcat. The first element in the termination region is an unusually large inverted repeat in the DNA (delta G = -71 kcal). The second element, 200 base pairs further downstream, is an RNA polymerase II promoter which directs transcription back upstream on the complementary strand. This transcription converges on and collides with that from the beta H gene at or near the inverted repeat where transcription from both directions stops. We propose that the inverted repeat is a strong pause site which positions the converging polymerases for mutual site-specific termination.

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48

Shin, Minsang, Arvin Cesar Lagda, Jae Woong Lee, Abhay Bhat, Joon Haeng Rhee, Jeong-Sun Kim, Kunio Takeyasu, and Hyon E. Choy. "Gene silencing by H-NS from distal DNA site." Molecular Microbiology 86, no. 3 (September 14, 2012): 707–19. http://dx.doi.org/10.1111/mmi.12012.

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49

Atlung, Tove, and Hanne Ingmer. "H‐NS: a modulator of environmentally regulated gene expression." Molecular Microbiology 24, no. 1 (April 1997): 7–17. http://dx.doi.org/10.1046/j.1365-2958.1997.3151679.x.

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50

Costanzo, F., M. Colombo, S. Staempfli, C. Santoro, M. Marone, R. Frank, H. Delius, and R. Cortese. "Structure of gene and pseudogenes of human apoferritin H." Nucleic Acids Research 14, no. 2 (January 26, 1986): 721–36. http://dx.doi.org/10.1093/nar/14.2.721.

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