Any process that activates or increases the frequency, rate or extent of I-kappaB kinase/NF-kappaB signaling.

Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an exogenous double-stranded RNA stimulus.

A change in morphology and behavior of a macrophage resulting from exposure to a cytokine, chemokine, cellular ligand, or soluble factor, leading to the initiation or perpetuation of an immune response.

Any series of molecular signals generated as a consequence of binding to a toll-like receptor not relying on the MyD88 adaptor molecule. Toll-like receptors directly bind pattern motifs from a variety of microbial sources to initiate innate immune response.

Any series of molecular signals generated as a consequence of binding to a toll-like receptor not relying on the MyD88 adaptor molecule. Toll-like receptors directly bind pattern motifs from a variety of microbial sources to initiate innate immune response.

The process in which a signal is passed on to downstream components within the cell through the I-kappaB-kinase (IKK)-dependent activation of NF-kappaB. The cascade begins with activation of a trimeric IKK complex (consisting of catalytic kinase subunits IKKalpha and/or IKKbeta, and the regulatory scaffold protein NEMO) and ends with the regulation of transcription of target genes by NF-kappaB. In a resting state, NF-kappaB dimers are bound to I-kappaB proteins, sequestering NF-kappaB in the cytoplasm. Phosphorylation of I-kappaB targets I-kappaB for ubiquitination and proteasomal degradation, thus releasing the NF-kappaB dimers, which can translocate to the nucleus to bind DNA and regulate transcription.

Any process that activates, maintains or increases the rate of autophagy. Autophagy is the process in which cells digest parts of their own cytoplasm.

Any process that activates, maintains or increases the rate of autophagy. Autophagy is the process in which cells digest parts of their own cytoplasm.

Any process that activates or increases the rate or extent of B cell proliferation.

Any process that activates or increases the frequency, rate or extent of the addition of ubiquitin groups to a protein.

A series of molecular signals initiated by the binding of a lipopolysaccharide (LPS) to a receptor on the surface of a target cell, and ending with regulation of a downstream cellular process, e.g. transcription. Lipopolysaccharides are major components of the outer membrane of Gram-negative bacteria, making them prime targets for recognition by the immune system.

Any process that activates or increases the frequency, rate or extent of protein binding.

Any process that activates or increases the frequency, rate, or extent of type I interferon production. Type I interferons include the interferon-alpha, beta, delta, episilon, zeta, kappa, tau, and omega gene families.

Any process that results in a change in state or activity of an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a lipopolysaccharide stimulus; lipopolysaccharide is a major component of the cell wall of gram-negative bacteria.

Any process that results in a change in state or activity of an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a lipopolysaccharide stimulus; lipopolysaccharide is a major component of the cell wall of gram-negative bacteria.

Any process that activates or increases the frequency, rate, or extent of interleukin-6 production.

Any process that activates or increases the frequency, rate, or extent of tumor necrosis factor production.

Any process that activates or increases the frequency, rate, or extent of tumor necrosis factor production.

Any process that activates or increases the frequency, rate, or extent of tumor necrosis factor production.

Any process that activates or increases the frequency, rate or extent of natural killer cell activation.

Any process that stops, prevents, or reduces the frequency, rate, or extent of MyD88-independent toll-like receptor signaling pathway.

Any series of molecular signals generated as a consequence of binding to a toll-like receptor where the TRIF adaptor mediates transduction of the signal. Toll-like receptors directly bind pattern motifs from a variety of microbial sources to initiate innate immune response.

Any series of molecular signals generated as a consequence of binding to a toll-like receptor where the TRIF adaptor mediates transduction of the signal. Toll-like receptors directly bind pattern motifs from a variety of microbial sources to initiate innate immune response.

Any series of molecular signals generated as a consequence of binding to a toll-like receptor where the TRIF adaptor mediates transduction of the signal. Toll-like receptors directly bind pattern motifs from a variety of microbial sources to initiate innate immune response.

Any process that activates or increases the frequency, rate or extent of I-kappaB kinase/NF-kappaB signaling.

Any process that activates or increases the frequency, rate or extent of I-kappaB kinase/NF-kappaB signaling.

Any process that activates or increases the frequency, rate or extent of I-kappaB kinase/NF-kappaB signaling.

Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an exogenous double-stranded RNA stimulus.

Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an exogenous double-stranded RNA stimulus.

Any process that modulates the frequency, rate or extent of protein homodimerization, interacting selectively with an identical protein to form a homodimer.

Any process that activates or increases the frequency, rate or extent of the chemical reactions and pathways resulting in the formation of chemokines.

Any process that activates or increases the frequency, rate or extent of the chemical reactions and pathways resulting in the formation of chemokines.

Any process that activates or increases the frequency, rate or extent of the chemical reactions and pathways resulting in the formation of interferon-beta.

Any process that activates or increases the frequency, rate or extent of the chemical reactions and pathways resulting in the formation of interferon-beta.

Any process that activates or increases the frequency, rate or extent of the chemical reactions and pathways resulting in the formation of nitric oxide.

Any process that activates or increases the frequency, rate or extent of B cell activation.

Any process that activates or increases the frequency, rate or extent of activity of the transcription factor NF-kappaB.

Any process that activates or increases the frequency, rate or extent of activity of the transcription factor NF-kappaB.

Reactions triggered in response to the presence of a virus that act to protect the cell or organism.

A programmed necrotic cell death process which begins when a cell receives a signal (e.g. a ligand binding to a death receptor or to a Toll-like receptor), and proceeds through a series of biochemical events (signaling pathways), characterized by activation of receptor-interacting serine/threonine-protein kinase 1 and/or 3 (RIPK1/3, also called RIP1/3) and by critical dependence on mixed lineage kinase domain-like (MLKL), and which typically lead to common morphological features of necrotic cell death. The process ends when the cell has died. The process is divided into a signaling phase, and an execution phase, which is triggered by the former.

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a lipopolysaccharide stimulus; lipopolysaccharide is a major component of the cell wall of gram-negative bacteria.

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a lipopolysaccharide stimulus; lipopolysaccharide is a major component of the cell wall of gram-negative bacteria.

A series of molecular signals which triggers the apoptotic death of a cell. The pathway starts with reception of a signal, and ends when the execution phase of apoptosis is triggered.

A series of molecular signals which triggers the apoptotic death of a cell. The pathway starts with reception of a signal, and ends when the execution phase of apoptosis is triggered.

A compound membranous cytoplasmic organelle of eukaryotic cells, consisting of flattened, ribosome-free vesicles arranged in a more or less regular stack. The Golgi apparatus differs from the endoplasmic reticulum in often having slightly thicker membranes, appearing in sections as a characteristic shallow semicircle so that the convex side (cis or entry face) abuts the endoplasmic reticulum, secretory vesicles emerging from the concave side (trans or exit face). In vertebrate cells there is usually one such organelle, while in invertebrates and plants, where they are known usually as dictyosomes, there may be several scattered in the cytoplasm. The Golgi apparatus processes proteins produced on the ribosomes of the rough endoplasmic reticulum; such processing includes modification of the core oligosaccharides of glycoproteins, and the sorting and packaging of proteins for transport to a variety of cellular locations. Three different regions of the Golgi are now recognized both in terms of structure and function: cis, in the vicinity of the cis face, trans, in the vicinity of the trans face, and medial, lying between the cis and trans regions.

The part of the cytoplasm that does not contain organelles but which does contain other particulate matter, such as protein complexes.

The lipid bilayer surrounding an endosome.

A protein complex whose core components are the receptor-interacting serine/threonine-protein kinases RIPK1 and RIPK3 (also called RIP1 and RIP3). Formation of the ripoptosome can induce an extrinsic apoptotic signaling pathway or a necroptotic signaling pathway. The composition of this protein complex may depend on several factors including nature of the signal, cell type and more.

A protein complex whose core components are the receptor-interacting serine/threonine-protein kinases RIPK1 and RIPK3 (also called RIP1 and RIP3). Formation of the ripoptosome can induce an extrinsic apoptotic signaling pathway or a necroptotic signaling pathway. The composition of this protein complex may depend on several factors including nature of the signal, cell type and more.