Academic literature on the topic 'C16orf35'
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Journal articles on the topic "C16orf35"
Zhou, Guo-Ling, Li Xin, Wei Song, Li-Jun Di, Guang Liu, Xue-Song Wu, De-Pei Liu, and Chih-Chuan Liang. "Active Chromatin Hub of the Mouse α-Globin Locus Forms in a Transcription Factory of Clustered Housekeeping Genes." Molecular and Cellular Biology 26, no. 13 (July 1, 2006): 5096–105. http://dx.doi.org/10.1128/mcb.02454-05.
Full textKowalczyk, Monika S., Jim R. Hughes, Jacqueline A. Sharpe, Jill M. Brown, Veronica J. Buckle, William G. Wood, and Douglas R. Higgs. "Does Transcription of Remote α-Globin Regulatory Elements Affect Their Function?." Blood 114, no. 22 (November 20, 2009): 4060. http://dx.doi.org/10.1182/blood.v114.22.4060.4060.
Full textLunardi, Andrea, Fulvio Chiacchiera, Elisa D’Este, Marcello Carotti, Marco Dal Ferro, Giulio Di Minin, Giannino Del Sal, and Licio Collavin. "The evolutionary conserved gene C16orf35 encodes a nucleo-cytoplasmic protein that interacts with p73." Biochemical and Biophysical Research Communications 388, no. 2 (October 2009): 428–33. http://dx.doi.org/10.1016/j.bbrc.2009.08.027.
Full textDu, Xinna, Wei Xia, Weiping Fan, Xuan Shen, Hongyan Wu, and Hu Zhang. "Integrated Analysis of C16orf54 as a Potential Prognostic, Diagnostic, and Immune Marker across Pan-Cancer." Disease Markers 2022 (September 9, 2022): 1–25. http://dx.doi.org/10.1155/2022/9365046.
Full textNakamura, Toru, Toyomasa Katagiri, Shoki Sato, Toshihiro Kushibiki, Koji Hontani, Takahiro Tsuchikawa, Satoshi Hirano, and Yusuke Nakamura. "Overexpression of C16orf74 is involved in aggressive pancreatic cancers." Oncotarget 8, no. 31 (July 28, 2016): 50460–75. http://dx.doi.org/10.18632/oncotarget.10912.
Full textAfink, Gijs B., Geertruda Veenboer, Janine de Randamie, Remco Keijser, Christof Meischl, Hans Niessen, and Carrie Ris-Stalpers. "Initial Characterization of C16orf89, A Novel Thyroid-Specific Gene." Thyroid 20, no. 7 (July 2010): 811–21. http://dx.doi.org/10.1089/thy.2009.0366.
Full textLi, Tingting, Fei Li, Jia Lin, Yinglan Zhang, Qi Zhang, Yanhe Sun, Xudong Chen, Mingqing Xu, Xu Wang, and Qiang Li. "Deletion of c16orf45 in zebrafish results in a low fertilization rate and increased thigmotaxis." Developmental Psychobiology 62, no. 8 (May 18, 2020): 1003–10. http://dx.doi.org/10.1002/dev.21984.
Full textBhalla, Kavita, Helen J. Eyre, Scott A. Whitmore, Grant R. Sutherland, and David F. Callen. "C16orf5, a novel proline-rich gene at 16p13.3, is highly expressed in the brain." Journal of Human Genetics 44, no. 6 (October 1999): 383–87. http://dx.doi.org/10.1007/s100380050183.
Full textArnold, A. W., P. H. Itin, M. Pigors, J. Kohlhase, L. Bruckner-Tuderman, and C. Has. "Poikiloderma with neutropenia: a novel C16orf57 mutation and clinical diagnostic criteria." British Journal of Dermatology 163, no. 4 (July 2, 2010): 866–69. http://dx.doi.org/10.1111/j.1365-2133.2010.09929.x.
Full textLu, Meng, Qin Xueying, Peng Hexiang, Gao Wenjing, Sara Hägg, Cao Weihua, Li Chunxiao, et al. "Genome-wide associations between alcohol consumption and blood DNA methylation: evidence from twin study." Epigenomics 13, no. 12 (June 2021): 939–51. http://dx.doi.org/10.2217/epi-2021-0039.
Full textDissertations / Theses on the topic "C16orf35"
Chiacchiera, Fulvio. "Characterization of a novel p63/p73 interacting protein." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2627.
Full textI tumori sono tra le maggiori cause di morte nelle popolazioni occidentali. D'altra parte anomalie congenite nello sviluppo nonostante non siano ugualmente frequenti richiedono uno sforzo notevole in termini di assistenza e cure da parte delle istituzioni e delle famiglie coinvolte. La comprensione dei processi molecolari alla base di queste patologie è quindi di fondamentale importanza per la medicina. Diverse evidenze sperimentali dimostrano come geni coinvolti nello sviluppo embrionale e nel differenziamento sono spesso coinvolto nella genesi dei tumori. In particolare membri della famiglia di p53 rivestono un ruolo fondamentale nell'omeostasi della cellula e le loro funzioni risultano spesso alterate nei tumori ed in alcune malattie genetiche. a livello molecolare l'attività di queste proteine è finemente regolata tramite una serie di modificazioni post-trascrizionali ed interazioni proteiche. Ogni singolo interattore risulta quindi un possibile bersaglio per nuove strategie farmacologiche. In questo lavoro presentiamo la caratterizzazione del prodotto del gene umano c16orf35, un nuovo interattore di p63e p73 isolato da uno screening volto a cercare nuovi interattori di p53 di Drosophila melanogaster. C16orf35 è una proteina nucleare evolutivamente molto conservata ed espressa ubiquitariamente. è in grado di associare con compartimenti cellulari specifici definiti "stress granules" e "p-bodies" in cui gli RNA subiscono diversi tipi di modificazioni strutturali. L'aumento forzato dei livelli cellulari di c16orf35 induce la formazione degli stress granules ed inibisce la proliferazione di cellule tumorali in coltura. Ciò suggerisce un possibile ruolo di questa proteina nelle vie che regolano la crescita cellulare.
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Jo, Adrienne. "Reduced Expression of Single 16p11.2 CNV Genes Alters Neuronal Morphology." Scholarship @ Claremont, 2019. https://scholarship.claremont.edu/cmc_theses/2091.
Full textBenslimane, Yahya. "Genome-wide CRISPR screens for the interrogation of genome integrity maintenance networks." Thesis, 2020. http://hdl.handle.net/1866/25540.
Full textThe genetic material (DNA) of an organism contains the necessary information for survival, growth and reproduction. Loss of this information strongly impacts the health of the organism and is the leading factor in aging and cancer. Almost all cells in an organism contain a copy of said genetic material (genome) and employ several mechanisms to repair any damaged section of the genome and to accurately copy it during cell division. We sought to understand the cellular processes by which cells maintain genome stability by systematically inactivating individual genes to uncover their role using pooled CRISPR-Cas9 screening. We employed genome-wide CRISPR screening in human cell lines in combination with specific chemical perturbations to identify gene deletions that enhance or suppress the phenotype of the chemical treatment, thereby shedding light on the effect of the treatment or the role of said enhancer/suppressor genes. We first focused on resveratrol; a small molecule first discovered in plants that has been suggested to extend lifespan in model organisms while also inhibiting cell proliferation ex vivo. Chemical-genetic screening pinpointed a role of resveratrol in inhibition of DNA replication. When we compared the cellular effects of resveratrol to hydroxyurea, a known inducer of replicative stress, we found that both treatments led to slower replication fork progression and activation of signaling in response to replicative stress. Importantly, we showed that the inhibition of DNA replication by resveratrol in human cells is a primary effect on cell proliferation and independent of the histone deacetylase Sirtuin-1, which has been implicated as the primary target in lifespan extension by resveratrol. We then studied the perturbation of a second cellular process, namely telomere maintenance. These specialized sequences at the termini of chromosomes are critical for the protection of chromosome ends and their erosion is counteracted by the enzymatic activity of telomerase. We performed a genome-wide CRISPR screen in cells that were concomitantly treated with a specific telomerase inhibitor, BIBR1532. We uncovered a strong genetic interaction between telomerase and a previously unannotated gene, C16orf72, which we named TAPR1. We found that TAPR1-depleted cells led to elevated p53 levels, a transcription factor central for the cellular response to telomeric and global DNA damage. We propose that TAPR1 is a negative regulator of p53 protein levels by promoting its turnover. Altogether, these studies highlight the power of CRISPR-Cas9 in genetic screening to uncover novel insight into the human genome stability maintenance network.