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What does X4 stand for?

X4 stands for CXCR4-dependent


This definition appears very rarely

See other definitions of X4

Samples in periodicals archive:

A dual role for the SDF-1/CXCR4 chemokine receptor system in adult brain: isoform-selective regulation of SDF-1 expression modulates CXCR4-dependent neuronal plasticity and cerebral leukocyte recruitment after focal ischemia. Stumm RK1, Rummel J, Junker V, Culmsee C, Pfeiffer M, Krieglstein J, Höllt V, Schulz S.
Chemokine receptor CXCR4-dependent internalization and resecretion of functional chemokine SDF-1 by bone marrow endothelial and stromal cells. Dar A1, Goichberg P, Shinder V, Kalinkovich A, Kollet O, Netzer N, Margalit R, Zsak M, Nagler A, Hardan I, Resnick I, Rot A, Lapidot T.
CXCR4-dependent cell migration in vitro and in vivo Cached.
Bertran, E. , Crosas-Molist, E. , Sancho, P. , Caja, L. , Lopez-Luque, J. , Navarro, E. , Egea, G. , Lastra, R. , Serrano, T. , Ramos, E. and Fabregat, I. (2013), Overactivation of the TGF-β pathway confers a mesenchymal-like phenotype and CXCR4-dependent migratory properties to liver tumor cells. Hepatology, 58: 2032–2044. doi: 10. 1002/hep.
Stromal cells regulate hematopoiesis by binding directly to hematopoietic precursors and providing numerous secreted factors. Stromal-derived factor (SDF-1) and its G protein–coupled chemokine receptor, CXCR4, are required for hematopoietic cell migration, adhesion, and bone marrow retention. 1-4 Mice lacking the chemokine SDF-1 or its receptor CXCR4 are unable to carry out normal hematopoiesis. 2,3 SDF-1–induced signaling pathways are defective in BCR-ABL–positive human leukemia cells and these disruptions contribute to the migration, adhesion, and retention of abnormalities characteristic of leukemia. 4,5 Intracellular signaling pathways that mediate CXCR4-dependent.
Although it was CD4 independent, the 92US143-T8 isolate also maintained the ability to infect CD4+ cells. In the present study, we investigated the role of CXCR4 in the infection of CD4+ and CD8+ cells by this primary isolate. The expression of CXCR4 was down modulated in CD8+ lymphocytes after infection with the 93US143-T8 isolate. Infection of CD8+ lymphocytes by the 93US143-T8 isolate was prevented by treatment with AMD3100, a specific antagonist for CXCR4, indicating CXCR4-dependent.