IndraLab

Statements


| 4 3

sparser
"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

reach
"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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"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]."

sparser
"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 )."

sparser
"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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"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."

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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."