Toll-Like Receptor Signaling Pathway ChIP PCR Array
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| The Human Toll-Like Receptor Signaling Pathway EpiTect ChIP qPCR Array profiles the histone modification status or “histone code” of 84 genes central to TLR-mediated signal transduction and innate immunity. Histone modifications regulate chromatin structure and correlate with the transcriptional activity of associated genes. The TLR family of pattern recognition receptors (PRRs) detects a wide range of bacteria, viruses, fungi and parasites via pathogen-associated molecular patterns (PAMPs). Each receptor binds to specific ligands, initiates a tailored innate immune response to the specific class of pathogen, and activates the adaptive immune response. For example, TLR4 recognizes bacterial lipopolysaccharide (LPS) or endotoxin, the compound which causes septic shock during blood-borne infection. The receptors act alone or as heterodimers, interacting with adaptor proteins to initiate MyD88 or TICAM1 (TRIF)-dependent responses. These responses initiate signaling cascades primarily through NF?B, which activates downstream JNK/p38 signaling or cytokine secretion. Dysregulation of these signaling pathways has severe consequences, and causes many autoimmune diseases and chronic pathological inflammation. This array includes members of the TLR signaling family as well as adaptor and effector proteins. Members of the NF?B, JNK/p38, IRF and JAK/STAT signaling pathways downstream of TLR activation are also included. Monitoring the histone modifications of these genes can help determine the epigenetic mechanisms controlling a model system’s ability to mount innate immune responses. Using chromatin immunoprecipitation and EpiTect ChIP qPCR Arrays, research studies can easily and reliably analyze the histone modification patterns associated with a focused gene panel related to TLR-mediated signal transduction. The EpiTect ChIP qPCR Arrays are intended for molecular biology applications. This product is not intended for the diagnosis, prevention, or treatment of a disease. |
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| Toll-Like Receptors: CD180 (LY64), SIGIRR, TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10. Pathogen-Specific Responses: Bacterial: CCL2 (MCP-1), CD14, CD180 (LY64), FOS, HRAS, IL10, IL12A, IL1B, IL6, IL8, IRAK1, HMGB1, JUN, LTA (TNFB), LY86 (MD-1), LY96, NFKBIA (IKBA/MAD3), PTGS2 (COX2), RELA, RIPK2, TLR2, TLR4, TLR6, TNFRSF1A, TICAM1 (TRIF). Viral: EIF2AK2 (PRKR), IFNB1, IFNG, IL12A, IL6, IRF3, PRKRA, RELA, TBK1, TLR3, TLR7, TLR8, TNF, TICAM1 (TRIF). Fungal/Parasitic: CLEC4E, HRAS, IL8, TLR2, TIRAP. TLR Signaling: Negative Regulation: SARM1, SIGIRR, TOLLIP. TICAM1 (TRIF)-Dependent (MYD88-Independent): IRF3, MAP3K7 (TAK1), MAP3K7IP1 (TAB1), NR2C2, PELI1, TBK1, TICAM2, TLR3, TLR4, TRAF6, TICAM1 (TRIF). MYD88-Dependent: IRAK1, IRAK2, MAP3K7 (TAK1), MAP3K7IP1 (TAB1), MYD88, NR2C2, TIRAP, TLR1, TLR10, TLR2, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TRAF6. Downstream Pathways and Target Genes: NF?B Pathway: BTK, CASP8, CHUK (IKKa), ECSIT (SITPEC), FADD, IKBKB, IL10, IL1B, IRAK1, IRAK2, IRF3, LY96, MAP3K7, MAP4K4, NFKB1, NFKB2, NFKBIA (IKBA/MAD3), NFKBIB, NFKBIL1, NFRKB, PPARA, REL, RELA, TNF, TNFRSF1A, UBE2N, UBE2V1. JNK/p38 Pathway: ELK1, FOS, IL1B, JUN, MAP2K3 (MEK3), MAP2K4 (JNKK1), MAP3K7, MAPK8 (JNK1), MAPK8IP3, MAPK9, TNF. JAK/STAT Pathway: CCL2 (MCP-1), CSF2 (GM-CSF), IFNG, IL12A, IL2, IL6. Interferon Regulatory Factor (IRF) Pathway: CXCL10 (INP10), IFNA1, IFNB1, IFNG, IRF1, IRF3, TBK1. Cytokine-Mediated Signaling Pathway: CCL2 (MCP-1), CSF3 (GCSF), IL1A, IL1B, IL6, IRAK1, IRAK2, RELA, SIGIRR, TNF, TNFRSF1A. Regulation of Adaptive Immunity: CD80, CD86, HSPD1, IFNG, IL10, IL12A, IL1B, IL2, MAP3K7, TRAF6. Adaptors & TLR Interacting Proteins: BTK, CD14, HMGB1, HRAS, HSPD1, LY86 (MD-1), LY96 (MD-2), MAPK8IP3, MYD88, PELI1, RIPK2, SARM1, TICAM1 (TRIF), TICAM2 (TRAM), TIRAP, TOLLIP. Effectors: CASP8 (FLICE), EIF2AK2 (PRKR), FADD, IRAK1, IRAK2, MAP3K7 (TAK1), MAP3K7IP1 (TAB1), NR2C2, PPARA, PRKRA, ECSIT (SITPEC), TRAF6, UBE2N, UBE2V1. |