排序方式: 共有285条查询结果,搜索用时 0 毫秒
51.
Řezáčová Veronika Slavíková Renata Zemková Lenka Konvalinková Tereza Procházková Věra Šťovíček Václav Hršelová Hana Beskid Olena Hujslová Martina Gryndlerová Hana Gryndler Milan Püschel David Jansa Jan 《Plant and Soil》2018,425(1-2):441-456
Plant and Soil - Although arbuscular mycorrhizal symbiosis is common in many plants with either C3 or C4 photosynthesis, it remains poorly understood whether photosynthesis type has any significant... 相似文献
52.
53.
54.
55.
Stefan Drie?en Niklas Berleth Olena Friesen Antje S L?ffler Philip B?hler Nora Hieke Fabian Stuhldreier Christoph Peter Kay O Schink Sebastian W Schultz Harald Stenmark Petter Holland Anne Simonsen Sebastian Wesselborg Bj?rn Stork 《Autophagy》2015,11(9):1458-1470
Autophagy represents an intracellular degradation process which is involved in both regular cell homeostasis and disease settings. In recent years, the molecular machinery governing this process has been elucidated. The ULK1 kinase complex consisting of the serine/threonine protein kinase ULK1 and the adapter proteins ATG13, RB1CC1, and ATG101, is centrally involved in the regulation of autophagy initiation. This complex is in turn regulated by the activity of different nutrient- or energy-sensing kinases, including MTOR, AMPK, and AKT. However, next to phosphorylation processes it has been suggested that ubiquitination of ULK1 positively influences ULK1 function. Here we report that the inhibition of deubiquitinases by the compound WP1130 leads to increased ULK1 ubiquitination, the transfer of ULK1 to aggresomes, and the inhibition of ULK1 activity. Additionally, WP1130 can block the autophagic flux. Thus, treatment with WP1130 might represent an efficient tool to inhibit the autophagy-initiating ULK1 complex and autophagy. 相似文献
56.
Nora Hieke Antje S L?ffler Takeshi Kaizuka Niklas Berleth Philip B?hler Stefan Drie?en Fabian Stuhldreier Olena Friesen Kaivon Assani Katharina Schmitz Christoph Peter Britta Diedrich J?rn Dengjel Petter Holland Anne Simonsen Sebastian Wesselborg Noboru Mizushima Bj?rn Stork 《Autophagy》2015,11(9):1471-1483
Autophagy describes an intracellular process responsible for the lysosome-dependent degradation of cytosolic components. The ULK1/2 complex comprising the kinase ULK1/2 and the accessory proteins ATG13, RB1CC1, and ATG101 has been identified as a central player in the autophagy network, and it represents the main entry point for autophagy-regulating kinases such as MTOR and AMPK. It is generally accepted that the ULK1 complex is constitutively assembled independent of nutrient supply. Here we report the characterization of the ATG13 region required for the binding of ULK1/2. This binding site is established by an extremely short peptide motif at the C terminus of ATG13. This motif is mandatory for the recruitment of ULK1 into the autophagy-initiating high-molecular mass complex. Expression of a ULK1/2 binding-deficient ATG13 variant in ATG13-deficient cells resulted in diminished but not completely abolished autophagic activity. Collectively, we propose that autophagy can be executed by mechanisms that are dependent or independent of the ULK1/2-ATG13 interaction. 相似文献
57.
S Jawhara E Pluskota D Verbovetskiy O Skomorovska-Prokvolit EF Plow DA Soloviev 《Journal of immunology (Baltimore, Md. : 1950)》2012,189(5):2468-2477
The opportunistic fungus Candida albicans is one of the leading causes of infections in immunocompromised patients, and innate immunity provides a principal mechanism for protection from the pathogen. In the present work, the role of integrin α(X)β(2) in the pathogenesis of fungal infection was assessed. Both purified α(X)β(2) and α(X)β(2)-expressing human epithelial kidney 293 cells recognized and bound to the fungal hyphae of SC5314 strain of C. albicans but not to the yeast form or to hyphae of a strain deficient in the fungal mannoprotein, Pra1. The binding of the integrin to the fungus was inhibited by β-glucans but not by mannans, implicating a lectin-like activity in recognition but distinct in specificity from that of α(M)β(2). Mice deficient in α(X)β(2) were more prone to systemic infection with the LD(50) fungal inoculum decreasing 3-fold in α(X)β(2)-deficient mice compared with wild-type mice. After challenging i.v. with 1.5 × 10(4) cell/g, 60% of control C57BL/6 mice died within 14 d compared with 100% mortality of α(X)β(2)-deficient mice within 9 d. Organs taken from α(X)β(2)-deficient mice 16 h postinfection revealed a 10-fold increase in fungal invasion into the brain and a 2-fold increase into the liver. These data indicate that α(X)β(2) is important for protection against systemic C. albicans infections and macrophage subsets in the liver, Kupffer cells, and in the brain, microglial cells use α(X)β(2) to control fungal invasion. 相似文献
58.
Rab GTPases function as essential regulators of vesicle transport in eukaryotic cells. MSS4 was shown to stimulate nucleotide exchange on Rab proteins associated with the exocytic pathway and to have nucleotide-free-Rab chaperone activity. A detailed kinetic analysis of MSS4 interaction with Rab8 showed that MSS4 is a relatively slow exchange factor that forms a long-lived nucleotide-free complex with RabGTPase. In contrast to other characterized exchange factor-GTPase complexes, MSS4:Rab8 complex binds GTP faster than GDP, but still ca. 3 orders of magnitude more slowly than comparable complexes. The crystal structure of the nucleotide-free MSS4:Rab8 complex revealed that MSS4 binds to the Switch I and interswitch regions of Rab8, forming an intermolecular beta-sheet. Complex formation results in dramatic structural changes of the Rab8 molecule, leading to unfolding of the nucleotide-binding site and surrounding structural elements, facilitating nucleotide release and slowing its rebinding. Coupling of nucleotide exchange activity to a cycle of GTPase unfolding and refolding represents a novel nucleotide exchange mechanism. 相似文献
59.
60.