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Wenting Dai, Quanjuan Wang, Fengqi Zhao, Jianxin Liu, Hongyun Liu
BACKGROUND: Bovine milk is an important nutrient source for humans. Forage plays a vital role in dairy husbandry via affecting milk quality and quantity. However, the differences in mammary metabolism of dairy cows fed different forages remain elucidated. In this study, we utilized transcriptomic RNA-seq and iTRAQ proteomic techniques to investigate and integrate the differences of molecular pathways and biological processes in the mammary tissues collected from 12 lactating cows fed corn stover (CS, low-quality, n = 6) and alfalfa hay (AH, high-quality, n = 6)...
May 29, 2018: BMC Genomics
Bona Lee, Kwiyeom Yoon, Sunghoon Lee, Jin Muk Kang, Junil Kim, Sung Han Shim, Hak-Min Kim, Sanghoon Song, Kazuhito Naka, An Keun Kim, Han-Kwang Yang, Seong-Jin Kim
Homozygous deletion is a frequent mutational mechanism of silencing tumor suppressor genes in cancer. Therefore, homozygous deletions have been analyzed for identification of tumor suppressor genes that can be utilized as biomarkers or therapeutic targets for cancer treatment. In this study, to elucidate potential tumor suppressor genes involved in gastric cancer (GC), we analyzed the entire set of large homozygous deletions in six human GC cell lines through genome- and transcriptome-wide approaches. We identified 51 genes in homozygous deletion regions of chromosomes and confirmed the deletion frequency in tumor tissues of 219 GC patients from The Cancer Genome Atlas database...
March 2015: Genes, Chromosomes & Cancer
James C Chen, Mariano J Alvarez, Flaminia Talos, Harshil Dhruv, Gabrielle E Rieckhof, Archana Iyer, Kristin L Diefes, Kenneth Aldape, Michael Berens, Michael M Shen, Andrea Califano
Identification of driver mutations in human diseases is often limited by cohort size and availability of appropriate statistical models. We propose a framework for the systematic discovery of genetic alterations that are causal determinants of disease, by prioritizing genes upstream of functional disease drivers, within regulatory networks inferred de novo from experimental data. We tested this framework by identifying the genetic determinants of the mesenchymal subtype of glioblastoma. Our analysis uncovered KLHL9 deletions as upstream activators of two previously established master regulators of the subtype, C/EBPβ and C/EBPδ...
October 9, 2014: Cell
Bajinder S Dhanoa, Tiziana Cogliati, Akhila G Satish, Elspeth A Bruford, James S Friedman
The Kelch-like (KLHL) gene family encodes a group of proteins that generally possess a BTB/POZ domain, a BACK domain, and five to six Kelch motifs. BTB domains facilitate protein binding and dimerization. The BACK domain has no known function yet is of functional importance since mutations in this domain are associated with disease. Kelch domains form a tertiary structure of β-propellers that have a role in extracellular functions, morphology, and binding to other proteins. Presently, 42 KLHL genes have been classified by the HUGO Gene Nomenclature Committee (HGNC), and they are found across multiple human chromosomes...
2013: Human Genomics
Sarah Maerki, Michael H Olma, Titu Staubli, Patrick Steigemann, Daniel W Gerlich, Manfredo Quadroni, Izabela Sumara, Matthias Peter
Cul3 (Cullin3)-based E3 ubiquitin ligases recently emerged as critical regulators of mitosis. In this study, we identify two mammalian BTB (Bric-a-brac-Tramtrack-Broad complex)-Kelch proteins, KLHL21 and KLHL22, that interact with Cul3 and are required for efficient chromosome alignment. Interestingly, KLHL21 but not KLHL22 is necessary for cytokinesis and regulates translocation of the chromosomal passenger complex (CPC) from chromosomes to the spindle midzone in anaphase, similar to the previously described BTB-Kelch proteins KLHL9 and KLHL13...
December 14, 2009: Journal of Cell Biology
F Lesueur, M de Lichy, M Barrois, G Durand, J Bombled, M-F Avril, A Chompret, F Boitier, G M Lenoir, B Bressac-de Paillerets, Monique Baccard, Bertrand Bachollet, Pascaline Berthet, Valérie Bonadona, Jean-Marie Bonnetblanc, Olivier Caron, Jacqueline Chevrant-Breton, Jean-François Cuny, Stéphane Dalle, Michèle Delaunay, Liliane Demange, Julie De Quatrebarbes, Jean-François Doré, Marc Frénay, Jean-Pierre Fricker, Marion Gauthier-Villars, Paul Gesta, Sophie Giraud, Philippe Gorry, Florent Grange, Andrew Green, Laetitia Huiart, Nicolas Janin, Pascal Joly, Delphine Kérob, Christine Lasset, Dominique Leroux, Jean-Marc Limacher, Michel Longy, Sandrine Mansard, Karine Marrou, Tanguy Martin-Denavit, Christine Mateus, Eve Maubec, Laurence Olivier-Faivre, Vincent Orlandini, Pascal Pujol, Bruno Sassolas, Dominique Stoppa-Lyonnet, Luc Thomas, Pierre Vabres, Laurence Venat, Ewa Wierzbicka, Hélène Zattara
Mutations in two genes encoding cell cycle regulatory proteins have been shown to cause familial cutaneous malignant melanoma (CMM). About 20% of melanoma-prone families bear a point mutation in the CDKN2A locus at 9p21, which encodes two unrelated proteins, p16(INK4a) and p14(ARF). Rare mutations in CDK4 have also been linked to the disease. Although the CDKN2A gene has been shown to be the major melanoma predisposing gene, there remains a significant proportion of melanoma kindreds linked to 9p21 in which germline mutations of CDKN2A have not been identified through direct exon sequencing...
July 22, 2008: British Journal of Cancer
Izabela Sumara, Matthias Peter
The spindle assembly checkpoint (SAC) is a mechanism that prevents premature chromosome segregation in anaphase before all chromosomes are correctly attached to the mitotic spindle. Errors in chromosome segregation lead to aneuploidy, which may be causally involved in tumorgenesis. Kinetochore complexes are the structural components of the SAC, which are tightly regulated by various mechanisms including phosphorylation and ubiquitin-dependent proteolysis. Recent studies shed new light on the regulatory pathways of the ubiquitin proteasome system involved in SAC signaling...
December 15, 2007: Cell Cycle
Izabela Sumara, Manfredo Quadroni, Claudia Frei, Michael H Olma, Grzegorz Sumara, Romeo Ricci, Matthias Peter
Faithful cell-cycle progression is tightly controlled by the ubiquitin-proteasome system. Here we identify a human Cullin 3-based E3 ligase (Cul3) which is essential for mitotic division. In a complex with the substrate-specific adaptors KLHL9 and KLHL13, Cul3 is required for correct chromosome alignment in metaphase, proper midzone and midbody formation, and completion of cytokinesis. This Cul3-based E3 ligase removes components of the chromosomal passenger complex from mitotic chromosomes and allows their accumulation on the central spindle during anaphase...
June 2007: Developmental Cell
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