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Yi Liu Michael J. Trnka Shenheng Guan Doyoung Kwon Do-Hyung Kim J.-J. Chen Peter A. Greer A. L. Burlingame Maria Almira Correia 《Molecular & cellular proteomics : MCP》2020,19(12):1968-1986
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- •Liver Mallory-Denk-Body inducers elicited an IκBα-loss and NF-κB-activation.
- •IκBα-loss was due to its sequestration into insoluble cytoplasmic aggregates.
- •Four proteomic approaches identified 10 IκBα-interacting/aggregating proteins.
- •Nup153/RanBP2-aggregation prevented IκBα nuclear entry for ending NF-κB-activation.
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Kai Bao Xiaofei Li Tetsuhiro Kajikawa Abe Toshiharu Nathalie Selevsek Jonas Grossmann George Hajishengallis Nagihan Bostanci 《Proteomics》2020,20(3-4)
Understanding the progression of periodontal tissue destruction is at the forefront of periodontal research. The authors aimed to capture the dynamics of gingival tissue proteome during the initiation and progression of experimental (ligature‐induced) periodontitis in mice. Pressure cycling technology (PCT), a recently developed platform that uses ultra‐high pressure to disrupt tissues, is utilized to achieve efficient and reproducible protein extraction from ultra‐small amounts of gingival tissues in combination with liquid chromatography‐tandem mass spectrometry (MS). The MS data are processed using Progenesis QI and the regulated proteins are subjected to METACORE, STRING, and WebGestalt for functional enrichment analysis. A total of 1614 proteins with ≥2 peptides are quantified with an estimated protein false discovery rate of 0.06%. Unsupervised clustering analysis shows that the gingival tissue protein abundance is mainly dependent on the periodontitis progression stage. Gene ontology enrichment analysis reveals an overrepresentation in innate immune regulation (e.g., neutrophil‐mediated immunity and antimicrobial peptides), signal transduction (e.g., integrin signaling), and homeostasis processes (e.g., platelet activation and aggregation). In conclusion, a PCT‐assisted label‐free quantitative proteomics workflow that allowed cataloging the deepest gingival tissue proteome on a rapid timescale and provided novel mechanistic insights into host perturbation during periodontitis progression is applied. 相似文献
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Sung‐Je Moon Jae‐Hoon Kim Young‐Keun Choi Chul‐Ho Lee Jung Hwan Hwang 《Journal of cellular and molecular medicine》2020,24(15):8814-8825
The growth arrest and DNA damage‐inducible beta (Gadd45β) protein have been associated with various cellular functions, but its role in progressive renal disease is currently unknown. Here, we examined the effect of Gadd45β deletion on cell proliferation and apoptosis, inflammation, and renal fibrosis in an early chronic kidney disease (CKD) mouse model following unilateral ureteral obstruction (UUO). Wild‐type (WT) and Gadd45β‐knockout (KO) mice underwent either a sham operation or UUO and the kidneys were sampled eight days later. A histological assay revealed that ablation of Gadd45β ameliorated UUO‐induced renal injury. Cell proliferation was higher in Gadd45β KO mouse kidneys, but apoptosis was similar in both genotypes after UUO. Expression of pro‐inflammatory cytokines after UUO was down‐regulated in the kidneys from Gadd45β KO mice, whereas UUO‐mediated immune cell infiltration remained unchanged. The expression of pro‐inflammatory cytokines in response to LPS stimulation decreased in bone marrow‐derived macrophages from Gadd45β KO mice compared with that in WT mice. Importantly, UUO‐induced renal fibrosis was ameliorated in Gadd45β KO mice unlike in WT mice. Gadd45β was involved in TGF‐β signalling pathway regulation in kidney fibroblasts. Our findings demonstrate that Gadd45β plays a crucial role in renal injury and may be a therapeutic target for the treatment of CKD. 相似文献