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Matches in Nanopublications for { ?s ?p "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." ?g. }

• _6 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.
• _5 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.
• _3 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.
• _6 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.
• _5 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.
• _5 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.
• _3 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.
• _5 value "Fig. 6 Model of TLR4 and chemokine receptor crosstalk. MIP-2 binding to CXCR2 induces PMN migration, as well as GRK2 and GRK5 expression, through PI3K-? signaling. Increased GRK2 and GRK5 expression results in chemokine receptor internalization and desensitization, thereby negatively regulating PMN migration. Thus, PI3K-?-activated signaling is postulated to be a feedback mechanism regulating PMN migration. Because persistent infection requires continued PMN infiltration, LPS acting through the TLR4 signaling pathway transcriptionally downregulates expression of GRK2 and GRK5 in response to MIP-2. This decreases chemokine receptor desensitization by preventing CXCR2 internalization and thus augments PMN migration. MEK kinase is involved in mediating the crosstalk between TLR4 and chemokine receptors. Dashed lines indicate inhibitory signals." provenance.