Pyroptosis PCR array
| 【Numbering】BKMI100014 | 【CAS】CAS | ||
| 【Item No.】BKMI100014-1 | 【specification】 | ||
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[Main Advantages]
Pyroptosis is mediated by inflammasome assembly, accompanied by GSDMD cleavage and the release of IL-1 β and IL-18. Inflammasomes are multimolecular complexes that are activated when the host is resistant to microbial infection and also promote adaptive developmental immune responses. Moreover, the inflammasome is also associated with non-microbial diseases. The assembly of inflammasomes begins with cytosolute pattern recognition receptors (PRR, also known as inflammasome sensors), which are capable of identifying pathogen-associated molecular patterns and risk-associated molecular patterns (PAMPs and DAMPs). Activation of PRRs promotes downstream signaling pathways and leads to type I interferon production and release of proinflammatory cytokines. PRRs form inflammatory bodies with pro-caspase-1 and ASC after the stimulation of cells by signaling molecules such as bacteria and viruses.
In the classical pathway, PAMPs and DAMPs receive intracellular signaling molecular stimulation and assemble with pro-caspase-1 and ASC to form the inflammasome and active caspase-1. Cleaved-caspase-1 cleaved GSDMD and pro-IL-1 β / 18. N-GSDMD penetrates the cell membrane by forming non-selective pores, further leading to water influx, lysis, and death. Furthermore, IL-1 β and IL-18 are secreted from the pores formed by the N-GSDMD.
In the nonclassical pathway, cytosolic LPS activates caspase-4 / 5 and caspase-11, triggering cellular pyroptosis by splitting the GSDMD. However, oxPAPC competes with LPS for binding to caspase-4 / 1, thereby inhibiting cell pyroptosis. Furthermore, cleavage of GSDMD causes K + efflux, which ultimately mediates the assembly of the NLRP 3 inflammasome, leading to cleavage of pro-IL-1 β and pro-IL-18. Activated caspase-11 also cleaves Pannexin-1 to induce ATP release and cell pyroptosis associated with P2X7R. In the caspase-3-mediated pathway, active caspase-3 cleaves GSDME to form N-GSDME and induce cell pyroptosis. In the caspase-8-mediated pathway, inhibition of TAK 1 induces the activation of caspase-8, which cleaves GSDMD and causes cell pyroptosis. Moreover, under hypoxia, PD-L1 is transferred to the nucleus and, together with p-Stat 3, regulates the transcription of GSDMC, leading to the conversion of apoptosis to pyroptosis after caspase-8 activation by TNF α. In the granzyme-mediated pathway, CART cells rapidly activate caspase-3 in target cells by the release of GzmB, and then GSDME is activated, causing extensive cell pyroptosis. Furthermore, GzmA and GzmB in cytotoxic lymphocytes enter the target cells via perforin and induce cell pyroptosis. GzmA hydrolyzes GSDMB, and GzmB directly activates GSDME.
Message
Pyroptosis is mediated by inflammasome assembly, accompanied by GSDMD cleavage and the release of IL-1 β and IL-18. Inflammasomes are multimolecular complexes that are activated when the host is resistant to microbial infection and also promote adaptive developmental immune responses. Moreover, the inflammasome is also associated with non-microbial diseases. The assembly of inflammasomes begins with cytosolute pattern recognition receptors (PRR, also known as inflammasome sensors), which are capable of identifying pathogen-associated molecular patterns and risk-associated molecular patterns (PAMPs and DAMPs). Activation of PRRs promotes downstream signaling pathways and leads to type I interferon production and release of proinflammatory cytokines. PRRs form inflammatory bodies with pro-caspase-1 and ASC after the stimulation of cells by signaling molecules such as bacteria and viruses.
In the classical pathway, PAMPs and DAMPs receive intracellular signaling molecular stimulation and assemble with pro-caspase-1 and ASC to form the inflammasome and active caspase-1. Cleaved-caspase-1 cleaved GSDMD and pro-IL-1 β / 18. N-GSDMD penetrates the cell membrane by forming non-selective pores, further leading to water influx, lysis, and death. Furthermore, IL-1 β and IL-18 are secreted from the pores formed by the N-GSDMD.
In the nonclassical pathway, cytosolic LPS activates caspase-4 / 5 and caspase-11, triggering cellular pyroptosis by splitting the GSDMD. However, oxPAPC competes with LPS for binding to caspase-4 / 1, thereby inhibiting cell pyroptosis. Furthermore, cleavage of GSDMD causes K + efflux, which ultimately mediates the assembly of the NLRP 3 inflammasome, leading to cleavage of pro-IL-1 β and pro-IL-18. Activated caspase-11 also cleaves Pannexin-1 to induce ATP release and cell pyroptosis associated with P2X7R. In the caspase-3-mediated pathway, active caspase-3 cleaves GSDME to form N-GSDME and induce cell pyroptosis. In the caspase-8-mediated pathway, inhibition of TAK 1 induces the activation of caspase-8, which cleaves GSDMD and causes cell pyroptosis. Moreover, under hypoxia, PD-L1 is transferred to the nucleus and, together with p-Stat 3, regulates the transcription of GSDMC, leading to the conversion of apoptosis to pyroptosis after caspase-8 activation by TNF α. In the granzyme-mediated pathway, CART cells rapidly activate caspase-3 in target cells by the release of GzmB, and then GSDME is activated, causing extensive cell pyroptosis. Furthermore, GzmA and GzmB in cytotoxic lymphocytes enter the target cells via perforin and induce cell pyroptosis. GzmA hydrolyzes GSDMB, and GzmB directly activates GSDME.
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