scholarly journals A Genome-wide Haploid Genetic Screen Identifies Regulators of Glutathione Abundance and Ferroptosis Sensitivity

Cell Reports ◽  
2019 ◽  
Vol 26 (6) ◽  
pp. 1544-1556.e8 ◽  
Author(s):  
Jennifer Yinuo Cao ◽  
Aunoy Poddar ◽  
Leslie Magtanong ◽  
Jennifer H. Lumb ◽  
Trevor R. Mileur ◽  
...  
Keyword(s):  
Genetic Screen ◽  
Genome Wide ◽  
A Genome

scholarly journals Novel skin phenotypes revealed by a genome-wide mouse reverse genetic screen

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Kifayathullah Liakath-Ali ◽  
Valerie E. Vancollie ◽  
Emma Heath ◽  
Damian P. Smedley ◽  
Jeanne Estabel ◽  
...  
Keyword(s):  
Genetic Screen ◽  
Reverse Genetic ◽  
Genome Wide ◽  
A Genome ◽  
Reverse Genetic Screen

scholarly journals Use of a genome-wide haploid genetic screen to identify treatment predicting factors: a proof-of-principle study in pancreatic cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (38) ◽  
pp. 63635-63645 ◽  
Author(s):  
Yuk Ting Ma ◽  
Sarah M. Leonard ◽  
Naheema Gordon ◽  
Jennifer Anderton ◽  
Claire James ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Genetic Screen ◽  
Predicting Factors ◽  
Genome Wide ◽  
A Genome ◽  
Proof Of Principle

scholarly journals Results of a genome-wide genetic screen for panic disorder

1998 ◽  
Vol 81 (2) ◽  
pp. 139-147 ◽  
Author(s):  
J.A. Knowles ◽  
A.J. Fyer ◽  
V.J. Vieland ◽  
M.M. Weissman ◽  
S.E. Hodge ◽  
...  
Keyword(s):  
Panic Disorder ◽  
Genetic Screen ◽  
Genome Wide ◽  
A Genome

Panic disorder is unlikely to be a homogeneous autosomal dominant disorder: Results of a genome-wide genetic screen

1996 ◽  
Vol 39 (7) ◽  
pp. 567
Author(s):  
J.A. Knowles ◽  
V.J. Vieland ◽  
M.M. Weissman ◽  
G. Heiman ◽  
G. de Jesus ◽  
...  
Keyword(s):  
Panic Disorder ◽  
Autosomal Dominant ◽  
Genetic Screen ◽  
Autosomal Dominant Disorder ◽  
Genome Wide ◽  
A Genome

scholarly journals A genome-wide genetic screen for host factors required for hepatitis C virus propagation

2009 ◽  
Vol 106 (38) ◽  
pp. 16410-16415 ◽  
Author(s):  
Q. Li ◽  
A. L. Brass ◽  
A. Ng ◽  
Z. Hu ◽  
R. J. Xavier ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Genetic Screen ◽  
Host Factors ◽  
Virus Propagation ◽  
Genome Wide ◽  
A Genome

scholarly journals Cross-talks of glycosylphosphatidylinositol biosynthesis with glycosphingolipid biosynthesis and ER-associated degradation

2019 ◽  
Author(s):  
Yicheng Wang ◽  
Yusuke Maeda ◽  
Yishi Liu ◽  
Yoko Takada ◽  
Akinori Ninomiya ◽  
...  
Keyword(s):  
Quality Control ◽  
Plasma Membranes ◽  
Genetic Screen ◽  
Side Chain ◽  
Gm1 Ganglioside ◽  
Er Quality Control ◽  
Functional Relationships ◽  
Genome Wide ◽  
A Genome ◽  
Glycosphingolipid Biosynthesis

Glycosylphosphatidylinositol (GPI)-anchored proteins and glycosphingolipids interact with each other in the mammalian plasma membranes, forming dynamic microdomains. How their interaction starts in the cells has been unclear. Here, based on a genome-wide CRISPR-Cas9 genetic screen for genes required for GPI side-chain modification by galactose in the Golgi apparatus, we report that β1,3-galactosyltransferase 4 (B3GALT4), also called GM1 ganglioside synthase, additionally functions in transferring galactose to the N-acetylgalactosamine side-chain of GPI. Furthermore, B3GALT4 requires lactosylceramide for the efficient GPI side-chain galactosylation. Thus, our work demonstrates previously unexpected evolutionary and functional relationships between GPI-anchored proteins and glycosphingolipids in the Golgi. Through the same screening, we also show that GPI biosynthesis in the endoplasmic reticulum (ER) is severely suppressed by ER-associated degradation to prevent GPI accumulation when the transfer of synthesized GPI to proteins is defective. Our data demonstrates cross-talks of GPI biosynthesis with glycosphingolipid biosynthesis and the ER quality control system.

Establishment of a genome-wide RNAi screen; Identification of novel genes involved in clonal maintenance of ALL

2014 ◽  
Vol 226 (03) ◽  
Author(s):  
F Ponthan ◽  
D Pal ◽  
J Vormoor ◽  
O Heidenreich
Keyword(s):  
Rnai Screen ◽  
Novel Genes ◽  
Genome Wide ◽  
A Genome

A genome-wide linkage scan for familial partial lipodystrophy susceptibility genes in a German kindreds

2007 ◽  
Vol 30 (4) ◽  
pp. 86
Author(s):  
M. Lanktree ◽  
J. Robinson ◽  
J. Creider ◽  
H. Cao ◽  
D. Carter ◽  
...  
Keyword(s):  
Subcutaneous Fat ◽  
Visceral Obesity ◽  
Fat Distribution ◽  
Dominant Negative ◽  
Molecular Forms ◽  
Partial Lipodystrophy ◽  
Genome Wide ◽  
A Genome ◽  
Familial Partial Lipodystrophy ◽  
Promoter Mutations

Background: In Dunnigan-type familial partial lipodystrophy (FPLD) patients are born with normal fat distribution, but subcutaneous fat from extremities and gluteal regions are lost during puberty. The abnormal fat distribution leads to the development of metabolic syndrome (MetS), a cluster of phenotypes including hyperglycemia, dyslipidemia, hypertension, and visceral obesity. The study of FPLD as a monogenic model of MetS may uncover genetic risk factors of the common MetS which affects ~30% of adult North Americans. Two molecular forms of FPLD have been identified including FPLD2, resulting from heterozygous mutations in the LMNA gene, and FPLD3, resulting from both heterozygous dominant negative and haploinsufficiency mutations in the PPARG gene. However, many patients with clinically diagnosed FPLD have no mutation in either LMNA or PPARG, suggesting the involvement of additional genes in FPLD etiology. Methods: Here, we report the results of an Affymetrix 10K GeneChip microarray genome-wide linkage analysis study of a German kindred displaying the FPLD phenotype and no known lipodystrophy-causing mutations. Results: The investigation identified three chromosomal loci, namely 1q, 3p, and 9q, with non-parametric logarithm of odds (NPL) scores >2.7. While not meeting the criteria for genome-wide significance, it is interesting to note that the 1q and 3p peaks contain the LMNA and PPARG genes respectively. Conclusions: Three possible conclusions can be drawn from these results: 1) the peaks identified are spurious findings, 2) additional genes physically close to LMNA, PPARG, or within 9q, are involved in FPLD etiology, or 3) alternative disease causing mechanisms not identified by standard exon sequencing approaches, such as promoter mutations, alternative splicing, or epigenetics, are also responsible for FPLD.

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