Information om | Engelska ordet CCR5

Exempel på hur man kan använda CCR5 i en mening

• C-C chemokine receptor type 5, also known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines.
• Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the beta-chemokine receptor CCR5 for entry and are thus able to replicate in macrophages and CD4+ T-cells.
• CCR5, a second receptor found on the surface of CD4+ cells and macrophages, called a chemokine co-receptor.
• Interleukin-8 receptor, RANTES receptors (CCR1, CCR3, CCR5), MIP-1 receptor, PF4 receptor, M-CSF receptor and NAP-2 receptor belong to GPCR chemokine receptor family.
• NK cells can be important source of CC chemokines and may suppress HIV infection by inhibition replication of HIV-1 virus by interfering with the ability to utilize CCR5 as a coreceptor for entry in CD4(+) cells.
• CCL13 induces chemotaxis in monocytes, eosinophils, T lymphocytes, and basophils by binding cell surface G-protein linked chemokine receptors such as CCR2, CCR3 and CCR5.
• HIV also requires a second co-receptor along with the CD4-gp120 complex to enter the target cells - either CCR5 or CXCR4.
• The two coreceptors involved in the entry of HIV-1, CCR5 and CXCR4, belong to the larger family of 7-transmembrane segment (7TM) G-protein coupled receptors.
• It is a post-attachment inhibitor, blocking HIV from binding to the CCR5 and CXCR4 co-receptors after HIV binds to the CD4 receptor on the surface of a CD4 cell.
• Inhibitors of CCR5, including DAPTA, prevent and reverse neurodegeneration and are therapeutic targets in stroke/brain injury and dementia, such as in Parkinsons Disease.
• By antagonizing the CXCR4 receptor, Tat also appears to selectively encourage the reproduction of less virulent M-tropic (macrophage-tropic) strains of HIV (which use the CCR5 receptor) early in the course of infection, allowing the more rapidly pathogenic T-tropic (T-cell-tropic) strains (which use the CXCR4 receptor) to emerge later after mutating from M-tropic strains.
• There has been some inquiry into the relationship between HHV-7 and HIV-1 co-receptors CXCR4 and CCR5.
• Viral entry to the CD4+ cell begins with attachment of the R5 HIV-1 glycoprotein 120 (gp120) to the CD4+ T-cell receptor, which produces a conformational change in gp120 and allows it to bind to CCR5, thereby triggering glycoprotein 41 (gp41) mediated fusion of the viral envelope with the cell membrane and the nucleocapsid enters the host cell (Figure 1).
• Then the virus binds to the chemokine coreceptors CXCR4 or CCR5, resulting in conformational changes in the envelope proteins.
• The CCR5 receptor isn't the only one that the virus uses as an entry point, some strains use the CXCR4 receptor for example, so even ignoring all impracticalities of this treatment other challenges would still need to be explored.
• This induces cardiomyocyte apoptosis either by signalling through CCR3, CCR5 or CXCR4, by entry into cardiomyocytes (after binding to ganglioside GM1), or through TNF-α.
• While the CCR5Δ32 deletion blocks the entry of virus strains that use the CCR5 receptor, the TNPO3 mutation causing LGMD1F blocks the CXCR4 receptor, making it effective on different HIV-1 strains, due to HIV tropism.
• Considering receptors, CCR3 and CCR5 are expressed in both lesional and nonlesional skin but CCR5 is higher in lesional skin.
• During this period, the Parmentier lab characterized the CCR5 GPCR and discovered its role as a co-receptor in HIV infection.
• Kanmogne and her colleagues discovered that the HIV-1 envelope glycoprotein, gp120, activates the CCR5 and CXCR4 receptors on the surface of human brain microvasculature endothelial cells (HBMECs) leading to toxicity and BBB leakage.

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