Protein involved in adaptive immunity. Vertebrates can develop a broad and almost infinite repertoire of antigen-specific receptors, which allows vertebrates to recognize almost any potential pathogen or toxin and to mount antigen-specific responses to it. Two types of adaptive immunity systems have evolved in vertebrates in order to generate immune receptor diversity. The jawed vertebrates strategy uses the V(D)JC recombination to achieve combinatorial diversity of immunoglobulin-based B cell receptors and T cell receptors. The jawless vertebrate strategy uses the somatic rearrangements of variable leucine-rich cassettes in the variable lymphocyte receptors (VLRs). The hallmarks of an adaptive immune system is the production of antigen-specific recognition receptor by somatic gene rearrangement. The long life of some antigen-primed cytotoxic lymphocytes and plasma cells provide protective memory to prevent reinvasion
Protein which contains at least one coiled coil domain, a type of secondary structure composed of two or more alpha helices which entwine to form a cable structure. In proteins, the helical cables serve a mechanical role in forming stiff bundles of fibres
Protein involved in innate immunity, an inborn defense mechanism used by organisms to defend themselves against invasion by pathogens (bacteria, fungi, viruses, etc.). Initially discovered in insects which are devoid of an adaptive immune system and rely only on innate immune reactions for their defense, this immediate response accomplishes many activities including recognition and effector functions. Recognition is mediated by broad specificity, pattern recognition, receptors which recognize many related molecular structures (e.g. polysaccharides, polynucleotides) present in microorganisms but not found in the host. The innate responses include the release of antimicrobial peptides, production of cytokines, acute- phase proteins, complement. Although many different innate immune mechanisms are deployed for host defence, a unifying theme of innate immunity is the use of germline-encoded pattern recognition receptors for pathogens or damaged self components, such as the Toll-like receptors, nucleotide-binding domain leucine-rich repeat (LRR)- containing receptors, retinoic acid-inducible gene I-like RNA helicases and C-type lectin receptors
Protein involved in immunity, any immune system process that functions in the response of an organism to a potential internal or invasive threat. The vertebrate immune system is formed by the innate immune system (composed of phagocytes, complement, antimicrobial peptides, etc) and by the adaptive immune system which consists of T- and B- lymphocytes
Protein involved in the generation of rhythmic pattern of behaviors or activities, e.g. circadian rhythm which is a metabolic or behavioural rhythm within a cycle of 24 hours
A glycoprotein produced in membrane-bound or secreted form by B lymphocytes. The basic structural unit of an immunoglobulin (Ig) is composed of two identical covalently linked heavy chains and two identical light chains. Both the heavy chains and light chains contain a series of repeating homologous structural units called Ig domains The N-terminal variable regions of the heavy and light chains form the antigen binding sites, whereas the C-terminal constant regions of the heavy chains interact with other molecules in the immune system. The membrane-bound antibodies serve as receptors that mediate the antigen- triggered activation of B cells. Secreted antibodies function as mediators of specific humoral immunity by engaging various effector mechanisms that serve to eliminate the bound antigen
Protein involved in the division of the embryo into segments and which is responsible for determining the internal polarity of the segments Segment polarity gene mutations are lethal and change the pattern and, often the polarity, of every segment
Protein which, if defective, causes Brugada syndrome, a heart disease characterized by an electrocardiogram pattern showing ST segment elevation in right precordial leads (V1 to V3), incomplete or complete right bundle branch block, and ventricular tachyarrhythmia. In some cases, tachycardia does not terminate spontaneously and it may degenerate into ventricular fibrillation and lead to sudden death
Protein encoded by the human immunodeficiency viruses HIV-1 or HIV-2, which are the cause of acquired immunodeficiency syndrome (AIDS). This disease is characterized by a severe defect of cell-mediated immunity which is often accompanied by cancers such as Kaposi's sarcoma, as well as secondary infections such as tuberculosis
Viral protein sharing sequence homology with host interleukins Interleukins are produced by immune system cells such as lymphocytes, macrophages and monocytes, and modulate inflammation and immunity by regulating growth, mobility and differentiation of lymphoid and other cells. Several viruses encode interleukin-like proteins playing a role in immune evasion. Additionally, viral interleukins have been shown to activate cellular signaling cascades that enhance virus replication
Viral protein involved in the inhibition of host NF-kappa-B. This protein is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. Many viruses have developed strategies to inhibit the NF-kappa-B pathway in order to evade host immunity and inhibit production of proinflammatory cytokines
Viral protein involved in the merging of the virus envelope with host endosomal membrane during viral penetration into host cell. Viral fusion proteins drive this fusion reaction by undergoing a major conformational change that is triggered by interactions with the target cell. The specific trigger is mainly endosome acidification which induce activation of the fusion protein by conformational change. This pathway is used by enveloped viruses which are endocytosed and whose fusion protein is usually pH-dependent like influenza A virus, rhabdoviruses, bornaviruses, filoviruses, asfarviridae, flaviviridae, alphaviruses, HIV-1, avian leukosis virus, SARS, 229E, and MHV-2 coronaviruses
Viral protein involved in the evasion of host adaptive immune response. Upon infection, the innate immune system provides mechanisms for the rapid sensing and elimination of viruses. Adaptive immunity has evolved to provide a broader and more finely tuned repertoire of recognition for both self- and nonself-antigens. A lot of viruses escape the adaptive immune response by different mechanisms including interference with the presentation of antigenic peptides at the surface of infected cells
Viral protein involved in the merging of the virus envelope with host cytoplasmic membrane during viral penetration into host cell. Virus fusion proteins drive this fusion reaction by undergoing a major conformational change that is triggered by interactions with the target cell. This pathway is used by viruses whose fusion protein is usually pH independent such as most paramyxoviruses, herpesviruses and retroviruses. MHV-JHM coronavirus has been shown to fuse directly with the host cytoplasmic membrane. Prokaryotic viruses such as Tectiviridae fuse their inner membrane with the host cytoplasmic membrane whereas Cystoviridae fuse their outer membrane with the host cytoplasmic membrane
Viral protein involved in the merging of the virion membrane with a host membrane during viral penetration into host cell. Viral fusion proteins drive this fusion reaction by undergoing a major conformational change that is triggered by interactions with the target cell. The specific trigger depends on the virus and can be exposure to low pH in the endocytic pathway or interaction of the virion with the host receptor(s). In prokaryotic viruses, host-virus membrane fusion can occur either at the host outer membrane or plasma membrane. Bacteriophages such as cystoviridae fuse their external envelope with the host outer membrane, whereas others like tectiviridae fuse their inner envelope with the host plasma membrane
Component of the inflammasome complex involved in innate immunity and inflammation. Inflammasomes are supramolecular micron-sized complexes that assemble in the cytosol adjacent to the nucleus in response to pathogens and other damage-associated signals. The core of inflammasomes consists of at least 2 components: a signal sensor and an effector inflammatory caspase (mostly CASP1). However, most inflammasomes contain a third element, an adaptor (often ASC/PYCARD) In response to a danger signal, the sensor homooligomerizes and interacts with the adaptor that polymerizes and forms a platform to recruit caspase precursors. This results in increased local concentration of the enzyme, leading to trans-autocleavage and activation. Active caspases process proinflammatory IL1B and IL18 cytokine precursors, which are then secreted in the extracellular milieu and induce inflammatory responses. In adaptor-independent inflammasomes, the sensor directly recruits the caspase. Additional proteins may interaction with the core complex. Inflammasomes also induce pyroptosis, an inflammatory form of programmed cell death
Protein synthesized or activated in the cell in response to viral infection, or protein with specific antiviral activity within the cell. Eukaryotic cells have an innate immune mechanism to fight viral infection, which is activated through the interferon signaling pathway or through dsRNA detection in the cytoplasm. It leads to the establishment of an antiviral cell state, which prevents virus replication or induces apoptosis. Most viruses have developed specific proteins to prevent the establishment of an antiviral state. About half of all bacteria and most archaea have a CRISPR (clustered regularly interspersed short plaindromic repeats) system of adaptive immunity to exogenous DNA. CRISPRs clusters are tandem arrays of alternating repeats and spacers, where the spacers in some cases are homologous to sequences from virus and plasmid genomes. The CRISPR arrays are transcribed, processed and in some way aid in detection and resistance to foreign DNA. In at least a few bacteria (E.coli, S.epidermidis) it seems DNA is the target, whereas in Pyrococcus furiosis it seems the CRISPR system targets RNA
Viral protein acting as an IgG Fc receptors, able to bind IgG and inhibit host Fc-dependent immune activation. Fc receptors are proteins found at the surface of certain cells of the immune system including macrophages, monocytes, natural killer cells or B-cells. They allow these cells to bind to antibodies that are attached to the surface of infected cells or pathogens, helping these cells to identify and eliminate pathogens
Protein involved in RNA-mediated gene silencing. This term describes a number of related processes which use 21- to 25-nucleotide RNAs to repress the expression of specific target genes. These processes include the post-transcriptional regulation of mRNA by either RNA interference (RNAi) or endogenously encoded microRNAs (miRNAs) and the transcriptional regulation of mRNA by RNAi-mediated chromatin silencing. RNAi is generally triggered by the presence of dsRNA produced by bidirectional transcription or by the transcription of an inverted repeat or hairpin sequence. dsRNA is processed into small interfering RNAs (siRNAs) of around 21 nucleotide which are then incorporated into the RNA-induced silencing complex (RISC), which cleaves mRNAs with sequences fully complementary to the siRNA. miRNAs differ from siRNAs principally in their biogenesis. miRNA genes encode precursors with complex hairpin structures which are processed by endonucleolytic cleavage to form mature miRNAs. Like siRNAs, miRNAs function in RISC-like complexes. Animal miRNAs generally inhibit translation of target mRNAs following imperfect base pairing to the 3'-untranslated region (3'-UTR), while most plant miRNAs show nearly precise complementarity to coding regions of target mRNAs and trigger mRNA degradation similar to siRNAs. Finally, in RNAi-mediated chromatin silencing, siRNAs derived from repeat element transcripts are incorporated into the nuclear RNAi-induced initiator of transcriptional silencing complex (RITS), where they guide chromatin modifications such as histone methylation which lead to transcriptional silencing
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