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971.
972.
Turner Alexandria Bond Danielle R. Vuong Quan V. Chalmers Anita Beckett Emma L. Weidenhofer Judith Scarlett Christopher J. 《Molecular biology reports》2020,47(3):2073-2084
Molecular Biology Reports - Treatment options for pancreatic cancer (PC) are severely limited due to late diagnosis, early metastasis and the inadequacy of chemotherapy and radiotherapy to combat... 相似文献
973.
Hernández-Ledesma Ana Laura Rodríguez-Méndez Adriana Jheny Gallardo-Vidal Lilia Susana García-Gasca Teresa Alatorre-Cruz Julia María García-Solís Pablo López Reyes Julián Solís-Saínz Juan Carlos 《Molecular biology reports》2020,47(12):9667-9676
Molecular Biology Reports - Although cognitive impairment (CI) is classically associated with aging, it has been proposed that neurological pathologies may increase the risk to suffer CI. Despite... 相似文献
974.
Bort Alicia Sánchez Belén G. de Miguel Irene Mateos-Gómez Pedro A. Diaz-Laviada Inés 《Molecular biology reports》2020,47(4):2635-2647
Molecular Biology Reports - According to the stem cell theory for cancer, hepatocellular carcinomas are sustained by a group of cancer stem cells (CSCs) which are responsible for resistance to... 相似文献
975.
Fressinaud Catherine Thomas Olivier Umerska Anita Monika Saulnier Patrick 《Neurochemical research》2020,45(11):2732-2748
Neurochemical Research - Promoting remyelination in multiple sclerosis is important to prevent axon degeneration, given the lack of curative treatment. Although some growth factors improve this... 相似文献
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977.
978.
Jenny Landberg Naia Risager Wright Tune Wulff Markus J. Herrgård Alex Toftgaard Nielsen 《Biotechnology and bioengineering》2020,117(12):3835-3848
Growth decoupling can be used to optimize the production of biochemicals and proteins in cell factories. Inhibition of excess biomass formation allows for carbon to be utilized efficiently for product formation instead of growth, resulting in increased product yields and titers. Here, we used CRISPR interference to increase the production of a single-domain antibody (sdAb) by inhibiting growth during production. First, we screened 21 sgRNA targets in the purine and pyrimidine biosynthesis pathways and found that the repression of 11 pathway genes led to the increased green fluorescent protein production and decreased growth. The sgRNA targets pyrF, pyrG, and cmk were selected and further used to improve the production of two versions of an expression-optimized sdAb. Proteomics analysis of the sdAb-producing pyrF, pyrG, and cmk growth decoupling strains showed significantly decreased RpoS levels and an increase of ribosome-associated proteins, indicating that the growth decoupling strains do not enter stationary phase and maintain their capacity for protein synthesis upon growth inhibition. Finally, sdAb production was scaled up to shake-flask fermentation where the product yield was improved 2.6-fold compared to the control strain with no sgRNA target sequence. An sdAb content of 14.6% was reached in the best-performing pyrG growth decoupling strain. 相似文献
979.
Alice Ward Racca Michael J. Rynkiewicz Nicholas LaFave Anita Ghosh William Lehman Jeffrey R. Moore 《The Journal of biological chemistry》2020,295(50):17128
Dilated cardiomyopathy (DCM) is associated with mutations in cardiomyocyte sarcomeric proteins, including α-tropomyosin. In conjunction with troponin, tropomyosin shifts to regulate actomyosin interactions. Tropomyosin molecules overlap via tropomyosin–tropomyosin head-to-tail associations, forming a continuous strand along the thin filament. These associations are critical for propagation of tropomyosin''s reconfiguration along the thin filament and key for the cooperative switching between heart muscle contraction and relaxation. Here, we tested perturbations in tropomyosin structure, biochemistry, and function caused by the DCM-linked mutation, M8R, which is located at the overlap junction. Localized and nonlocalized structural effects of the mutation were found in tropomyosin that ultimately perturb its thin filament regulatory function. Comparison of mutant and WT α-tropomyosin was carried out using in vitro motility assays, CD, actin co-sedimentation, and molecular dynamics simulations. Regulated thin filament velocity measurements showed that the presence of M8R tropomyosin decreased calcium sensitivity and thin filament cooperativity. The co-sedimentation of actin and tropomyosin showed weakening of actin-mutant tropomyosin binding. The binding of troponin T''s N terminus to the actin-mutant tropomyosin complex was also weakened. CD and molecular dynamics indicate that the M8R mutation disrupts the four-helix bundle at the head-to-tail junction, leading to weaker tropomyosin–tropomyosin binding and weaker tropomyosin–actin binding. Molecular dynamics revealed that altered end-to-end bond formation has effects extending toward the central region of the tropomyosin molecule, which alter the azimuthal position of tropomyosin, likely disrupting the mutant thin filament response to calcium. These results demonstrate that mutation-induced alterations in tropomyosin–thin filament interactions underlie the altered regulatory phenotype and ultimately the pathogenesis of DCM. 相似文献
980.
Ernetti Julia R. Boschetti Joana P. Delazeri Francieli De Bastiani Veluma I. M. Pontes Mariana R. Ribeiro Luisa P. Lingnau Rodrigo Toledo Luís Felipe Lucas Elaine M. 《Hydrobiologia》2020,847(16):3355-3364
Hydrobiologia - Pithecopus rusticus is an endemic amphibian restricted to the type locality, in southern Brazil, and possibly endangered to extinction, due to habitat degradation. However, an... 相似文献