Asc Adaptor Protein
Asc Adaptor Protein - Related Videos
07:48
Engineering a Bilayered Hydrogel to Control ASC Differentiation
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Cited by 12 •
2012
This protocol focuses on utilizing the inherent ability of stem cells to take cue from their surrounding extracellular matrix and be induced to differentiate into multiple phenotypes. This methods manuscript extends our description and characterization of a model utilizing a bilayered hydrogel, composed of PEG-fibrin and collagen, to simultaneously co-differentiate adipose-derived stem cells1.
17:14
In vivo and in vitro Studies of Adaptor-clathrin Interaction
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Cited by 8 •
2011
Clathrin-mediated endocytosis depends on adaptor proteins that coordinate cargo selection and clathrin coat assembly. Here we describe procedures to study adaptor-clathrin physical interaction and live cell imaging approaches using as a model the yeast endocytic adaptor protein Sla1p.
08:46
Green Fluorescent Protein-based Expression Screening of Membrane Proteins in Escherichia coli
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Cited by 34 •
2015
A streamlined approach to screening for the expression of recombinant membrane proteins in Escherichia coli based on fusion to green fluorescent protein is presented.
02:54
Protein Kinases and Phosphatases
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2020
Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven. Protein kinases Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
08:52
Immunomagnetic Separation of Fat Depot-specific Sca1high Adipose-derived Stem Cells (ASCs)
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Cited by 2 •
2016
We present the techniques required to isolate the stromal vascular fraction (SVF) from mouse inguinal (subcutaneous) and perigonadal (visceral) adipose tissue depots to assess their gene expression and collagenolytic activity. This method includes the enrichment of Sca1high adipose-derived stem cells (ASCs) using immunomagnetic cell separation.
FAQs
The two-domain architecture of ASC adaptor protein enables sequential signal transfer. Its pyrin domain associates with an activated inflammasome sensor, while its CARD provides a platform for filament formation and pro-caspase-1 recruitment. This arrangement concentrates the protease precursor within the signaling complex, connecting danger detection to downstream inflammatory processing rather than producing an isolated receptor response.
ASC filaments organize multiple CARD-containing signaling interactions in a common inflammasome structure. By recruiting pro-caspase-1 into this assembled complex, ASC supports the activation step needed for processing interleukin-1β and interleukin-18. The resulting organization helps explain how a danger-sensing event is converted into coordinated cytokine maturation and inflammatory cell death.
ASC occupies an intermediate position between detection and response. An inflammasome sensor recognizes an activated danger state, whereas ASC connects that sensor to pro-caspase-1 through its pyrin and CARD domains. Caspase-1 and the cytokines it processes act downstream as effectors. This division of roles allows sensing, assembly, and inflammatory output to remain functionally distinct.
A conceptual analysis follows the pathway from sensor activation to ASC recruitment, filament assembly, and pro-caspase-1 incorporation. Investigators then consider caspase-1 activation, processing of interleukin-1β and interleukin-18, and possible pyroptosis. Tracking these linked stages helps connect an initiating danger signal with the specific inflammatory outcomes attributed to the assembled inflammasome.
ASC adaptor protein provides a framework for studying how innate immune systems respond to pathogens. Its position between danger sensing and caspase-1 activation allows researchers to examine how infection-related signals produce inflammatory cytokine maturation and pyroptosis. This is relevant to understanding host defense, while also considering how excessive or misdirected activation may contribute to inflammatory disease.
Studies can evaluate whether inflammasome assembly is linked to caspase-1 activation, interleukin-1β and interleukin-18 processing, or pyroptotic cell death. Examining these outcomes together helps clarify whether a response proceeds from sensing through inflammatory effector events. Such information supports investigation of dysregulated inflammation and the development of approaches aimed at inflammasome-driven disease pathways.