Inflammasomes, multi-cellular protein complex in myeloid cells, induce several metabolic diseases via interleukin-1β maturation

2013 ◽  
Vol 14 (4) ◽  
pp. 195-200 ◽  
Author(s):  
Geun-Shik Lee ◽  
Keyword(s):  
Protein Complex ◽  
Metabolic Diseases ◽  
Myeloid Cells ◽  
Cellular Protein ◽  
Interleukin 1Β

Development of Deuterated-leucine Labeling with Immunoprecipitation to Analyze Cellular Protein Complex

2008 ◽  
Vol 01 (06) ◽  
pp. 293-301 ◽  
Author(s):  
Shufang Liang ◽  
Xuejiao Xu ◽  
Haojie Lu ◽  
Pengyuan Yang
Keyword(s):  
Protein Complex ◽  
Cellular Protein

scholarly journals Myeloid cells in COVID-19 microenvironment

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Guohui Qin ◽  
Shasha Liu ◽  
Li Yang ◽  
Weina Yu ◽  
Yi Zhang
Keyword(s):  
Cerebrospinal Fluid ◽  
Autoimmune Diseases ◽  
Peripheral Blood ◽  
Therapeutic Strategy ◽  
Metabolic Diseases ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Driving Factor ◽  
Single Cell Sequencing ◽  
Promote Disease Progression

AbstractVarying differentiation of myeloid cells is common in tumors, inflammation, autoimmune diseases, and metabolic diseases. The release of cytokines from myeloid cells is an important driving factor that leads to severe COVID-19 cases and subsequent death. This review briefly summarizes the results of single-cell sequencing of peripheral blood, lung tissue, and cerebrospinal fluid of COVID-19 patients and describes the differentiation trajectory of myeloid cells in patients. Moreover, we describe the function and mechanism of abnormal differentiation of myeloid cells to promote disease progression. Targeting myeloid cell-derived cytokines or checkpoints is essential in developing a combined therapeutic strategy for patients with severe COVID-19.

scholarly journals Regulation of protein complex partners as a compensatory mechanism in aneuploid tumors

2021 ◽  
Author(s):  
Gökçe Senger ◽  
Stefano Santaguida ◽  
Martin H Schaefer
Keyword(s):  
Protein Degradation ◽  
Protein Complex ◽  
Transcriptional Control ◽  
Patient Survival ◽  
Cellular Protein ◽  
The Other ◽  
Compensatory Mechanism ◽  
Proteomic Data ◽  
Chromosome Imbalance ◽  
Chromosome Level

Aneuploidy, a state of chromosome imbalance, is a hallmark of human tumors, but its role in cancer still remains to be fully elucidated. To understand the consequences of whole chromosome-level aneuploidies on the proteome, we integrated aneuploidy, transcriptomic and proteomic data from hundreds of TCGA/CPTAC tumor samples. We found a surprisingly large number of expression changes happened on other, non-aneuploid chromosomes. Moreover, we identified an association between those changes and co-complex members of proteins from aneuploid chromosomes. This co-abundance association is tightly regulated for aggregation-prone aneuploid proteins and those involved in a smaller number of complexes. On the other hand, we observe that complexes of the cellular core machinery are under functional selection to maintain their stoichiometric balance in aneuploid tumors. Ultimately, we provide evidence that those compensatory and functional maintenance mechanisms are established through post-transcriptional control and that the degree of success of a tumor to deal with aneuploidy-induced stoichiometric imbalance impacts the activation of cellular protein degradation programs and patient survival.

scholarly journals Protein Quality Control and Lipid Droplet Metabolism

2020 ◽  
Vol 36 (1) ◽  
pp. 115-139 ◽  
Author(s):  
Melissa A. Roberts ◽  
James A. Olzmann
Keyword(s):  
Quality Control ◽  
Protein Quality ◽  
Metabolic Diseases ◽  
Neutral Lipids ◽  
Protein Quality Control ◽  
Cellular Protein ◽  
Nutrient Sensing ◽  
Nonalcoholic Fatty Liver ◽  
Triacylglycerol Synthesis ◽  
Associated Proteins

Lipid droplets (LDs) are endoplasmic reticulum–derived organelles that consist of a core of neutral lipids encircled by a phospholipid monolayer decorated with proteins. As hubs of cellular lipid and energy metabolism, LDs are inherently involved in the etiology of prevalent metabolic diseases such as obesity and nonalcoholic fatty liver disease. The functions of LDs are regulated by a unique set of associated proteins, the LD proteome, which includes integral membrane and peripheral proteins. These proteins control key activities of LDs such as triacylglycerol synthesis and breakdown, nutrient sensing and signal integration, and interactions with other organelles. Here we review the mechanisms that regulate the composition of the LD proteome, such as pathways that mediate selective and bulk LD protein degradation and potential connections between LDs and cellular protein quality control.

scholarly journals Rapid extraction and kinetic analysis of protein complexes from single cells

2021 ◽  
Author(s):  
Sena Sarıkaya ◽  
Daniel J Dickinson
Keyword(s):  
Single Molecule ◽  
Protein Complex ◽  
Cell Biology ◽  
Dynamic Range ◽  
Protein Complexes ◽  
Single Cells ◽  
Cell Lysis ◽  
Cellular Protein ◽  
In Vitro Assays

Proteins contribute to cell biology by forming dynamic, regulated interactions, and measuring these interactions is a foundational approach in biochemistry. We present a rapid, quantitative in vivo assay for protein-protein interactions, based on optical cell lysis followed by time-resolved single-molecule analysis of protein complex binding to an antibody-coated substrate. We show that our approach has better reproducibility, higher dynamic range, and lower background than previous single-molecule pull-down assays. Furthermore, we demonstrate that by monitoring cellular protein complexes over time after cell lysis, we can measure the dissociation rate constant of a cellular protein complex, providing information about binding affinity and kinetics. Our dynamic single-cell, single-molecule pull-down method thus approaches the biochemical precision that is often sought from in vitro assays, while being applicable to native protein complexes isolated from single cells in vivo.

scholarly journals Prkaa1 Metabolically Regulates Monocyte/Macrophage Recruitment and Viability in Diet-Induced Murine Metabolic Disorders

2021 ◽  
Vol 8 ◽  
Author(s):  
Qiuhua Yang ◽  
Qian Ma ◽  
Jiean Xu ◽  
Zhiping Liu ◽  
Jianqiu Zou ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Myeloid Cells ◽  
Glucose And Lipid Metabolism ◽  
Atherosclerotic Lesions ◽  
Its Gene ◽  
Metabolic Sensor ◽  
Amp Activated Protein Kinase ◽  
Macrophage Viability

Myeloid cells, including monocytes/macrophages, primarily rely on glucose and lipid metabolism to provide the energy and metabolites needed for their functions and survival. AMP-activated protein kinase (AMPK, its gene is PRKA for human, Prka for rodent) is a key metabolic sensor that regulates many metabolic pathways. We studied recruitment and viability of Prkaa1-deficient myeloid cells in mice and the phenotype of these mice in the context of cardio-metabolic diseases. We found that the deficiency of Prkaa1 in myeloid cells downregulated genes for glucose and lipid metabolism, compromised glucose and lipid metabolism of macrophages, and suppressed their recruitment to adipose, liver and arterial vessel walls. The viability of macrophages in the above tissues/organs was also decreased. These cellular alterations resulted in decreases in body weight, insulin resistance, and lipid accumulation in liver of mice fed with a high fat diet, and reduced the size of atherosclerotic lesions of mice fed with a Western diet. Our results indicate that AMPKα1/PRKAA1-regulated metabolism supports monocyte recruitment and macrophage viability, contributing to the development of diet-induced metabolic disorders including diabetes and atherosclerosis.

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