IndraLab

Statements


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"The invasive behavior of cancer cells might indirectly depend on locally released CXCL2 that, via an autocrine mechanism, binds to CXCR4 impairing chemotaxis towards CXCL12 producing target organs and metastatic spread [XREF_BIBR]."

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"However, AdMIP-2 infection in mice lacking the CXC chemokine receptor that binds MIP-2, CXCR2, did not attenuate any of the markers of liver injury after adenovirus and acetaminophen challenge."

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"PGE 2 also augments the expression of chemokines CXCR4 on HSPCs and CXCL12 in nearby stromal cells, and CXCR4-CXCL2 interaction is essential for HSC quiescence ( xref )."

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"The chemotaxis of MDSCs is driven by gradients of the chemokines CXCL1, CXCL2, CXCL5, CXCL8, and CXCL12, which bind to their cognate receptors CXCR1, CXCR2, and CXCR4, on MDSCs; the chemotaxis of TAMs[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"By attaching CXCR4 to tumor cells, the CXCR4-CXCL2 axis can use its surroundings to keep neoplastic cells growing and surviving [19] ."

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"Matrix metalloproteinases promote leukemic cell invasion and transendothelial migration and are activated by integrin signaling, CXCL2 and CXCR4 interaction and ERK pathway activation."

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"showed that the CXCL2 and CXCR4 interaction binds breast cancer cells to microenvironment of the bone marrow and that CXCR4 inhibition prevents metastatic progression."

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"Materials and Methods: In silico approaches including homology modeling, molecular docking, molecular dynamic simulations and binding free energy calculations were employed on the study of the binding of CXCL2 to CXCR4, and in vitro surface plasmon resonance measurement, peptide/cell adhesion, transmigration assays were applied for the validations of the in silico results."
| PMC

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"In addition, interactions related to cell adhesion such as MDK–SDC4 and cytokine interactions such as CXCL2CXCR4 were observed ( xref )."

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"In tumor cells expressing a high level of CXCR4, the disruption of the CXCR4-CXCL2 interaction induces a diminution of the interactions of cancer cells with the bone marrow environment."

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"Fig. 2 depicts how the CXCR4-CXCL2 axis contributes to the melanoma microenvironment and promotes metastasis."

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"21 The low expression of CXCL12 in breast tumor tissue and high expression of CXCL12 at the metastatic sites creates a CXCl2-CXCR4 gradient which induces organotropism and a direction for the migratio[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Subsequent studies have demonstrated that the CXCR4 and CXCL2 interaction plays a central role in mediating neutrophil release without the requirement of other signalling pathways, such as Toll like receptor (TLR) 4, myeloid differentiation primary response gene (MyD) 88 or TIR domain containing adaptor inducing interferon-beta (TRIF) 45."