211. |
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212. |
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213. |
- Vieira, Natassia M., et al.
(författare)
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Jagged 1 Rescues the Duchenne Muscular Dystrophy Phenotype
- 2015
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Ingår i: Cell. - : Elsevier BV. - 0092-8674 .- 1097-4172. ; 163:5, s. 1204-1213
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Tidskriftsartikel (refereegranskat)abstract
- Duchenne muscular dystrophy (DMD), caused by mutations at the dystrophin gene, is the most common form of muscular dystrophy. There is no cure for DMD and current therapeutic approaches to restore dystrophin expression are only partially effective. The absence of dystrophin in muscle results in dysregulation of signaling pathways, which could be targets for disease therapy and drug discovery. Previously, we identified two exceptional Golden Retriever muscular dystrophy (GRMD) dogs that are mildly affected, have functional muscle, and normal lifespan despite the complete absence of dystrophin. Now, our data on linkage, whole-genome sequencing, and transcriptome analyses of these dogs compared to severely affected GRMD and control animals reveals that increased expression of Jagged1 gene, a known regulator of the Notch signaling pathway, is a hallmark of the mild phenotype. Functional analyses demonstrate that Jagged1 overexpression ameliorates the dystrophic phenotype, suggesting that Jagged1 may represent a target for DMD therapy in a dystrophin-independent manner.
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214. |
- Volz, Erik, et al.
(författare)
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Evaluating the Effects of SARS-CoV-2 Spike Mutation D614G on Transmissibility and Pathogenicity
- 2021
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Ingår i: Cell. - : Elsevier BV. - 1097-4172 .- 0092-8674. ; 184:1, s. 11-75
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Tidskriftsartikel (refereegranskat)abstract
- Global dispersal and increasing frequency of the SARS-CoV-2 spike protein variant D614G are suggestive of a selective advantage but may also be due to a random founder effect. We investigate the hypothesis for positive selection of spike D614G in the United Kingdom using more than 25,000 whole genome SARS-CoV-2 sequences. Despite the availability of a large dataset, well represented by both spike 614 variants, not all approaches showed a conclusive signal of positive selection. Population genetic analysis indicates that 614G increases in frequency relative to 614D in a manner consistent with a selective advantage. We do not find any indication that patients infected with the spike 614G variant have higher COVID-19 mortality or clinical severity, but 614G is associated with higher viral load and younger age of patients. Significant differences in growth and size of 614G phylogenetic clusters indicate a need for continued study of this variant.
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215. |
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216. |
- Wallberg-Henriksson, H, et al.
(författare)
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A new twist on brown fat metabolism
- 2009
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Ingår i: Cell. - : Elsevier BV. - 1097-4172 .- 0092-8674. ; 137:1, s. 22-24
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Tidskriftsartikel (refereegranskat)
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217. |
- Walldén, Mats, et al.
(författare)
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The Synchronization of Replication and Division Cycles in Individual E. coli Cells
- 2016
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Ingår i: Cell. - : Elsevier BV. - 0092-8674 .- 1097-4172. ; 166:3, s. 729-739
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Tidskriftsartikel (refereegranskat)abstract
- Isogenic E. coli cells growing in a constant environment display significant variability in growth rates, division sizes, and generation times. The guiding principle appears to be that each cell, during one generation, adds a size increment that is uncorrelated to its birth size. Here, we investigate the mechanisms underlying this "adder'' behavior by mapping the chromosome replication cycle to the division cycle of individual cells using fluorescence microscopy. We have found that initiation of chromosome replication is triggered at a fixed volume per chromosome independent of a cell's birth volume and growth rate. Each initiation event is coupled to a division event after a growth-rate-dependent time. We formalize our findings in a model showing that cell-to-cell variation in division timing and cell size is mainly driven by variations in growth rate. The model also explains why fast-growing cells display adder behavior and correctly predict deviations from the adder behavior at slow growth.
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218. |
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219. |
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220. |
- Weinberg, R. A., et al.
(författare)
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All You Need Is Mentorship
- 2016
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Ingår i: Cell. - : Elsevier BV. - 0092-8674 .- 1097-4172. ; 164:6, s. 1092-1093
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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