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Dating origin ccr5 delta32

However, CCR5 mutations are not likely to be the unique mechanism of protection because HIV-1 variants can use other chemokine receptors as their coreceptor and, indeed, infection has been demonstrated within the presence of such mutations.9520457, images] [Full Text]" pmid="9520457"Zagury et al.

The HIV-1 envelope glycoprotein gp120 interacts consecutively with CD4 and the CCR5 coreceptor to mediate the entry of certain HIV-1 strains into target cells.

10823934, images] [Full Text]" pmid="10823934"Cormier et al.

Both groups showed that expression of the CCCKR5 protein renders nonpermissive CD4 cells susceptible to infection by HIV-1 strains (see 609423).

8658171] [Full Text]" pmid="8658171"Alkhatib et al. (1996) reported similar observations and detected m RNA for the receptor only in cell types susceptible to macrophage-tropic isolates of HIV-1.

The 2 coding regions share 75% DNA and amino acid sequence identity. (1997) analyzed the genomic structure of CCR5, which contains 4 exons, spanning approximately 6 kb, and only 2 introns. Exon 4 contains the open reading frame, the complete 3-prime UTR, and 11 nucleotides of the 5-prime UTR.

Dating origin ccr5 delta32

Transcripts are initiated from 2 distinct promoters, both of which are AT-rich and lack canonical TATA or CAAT motifs; one is upstream of exon 1 and the other downstream, including the 'intronic' region between exons 1 and 3.Complex alternative splicing patterns in the 5-prime UTR and in the 4 exons give rise to multiple CCR5 transcripts.The regulatory sequences and noncoding exons are polymorphic, whereas the protein sequence is not. (1998) showed that polarized Th1 cells preferentially express CXCR3 (300574) and CCR5.Sulfated tyrosines contributed to the binding of CCR5 to MIP-1-alpha, MIP-1-beta, and HIV-1 gp120/CD4 complexes, and to the ability of HIV-1 to enter cells expressing CCR5 and CD4.10089882] [Full Text]" pmid="10089882"Farzan et al. (1999) concluded that tyrosine sulfation may contribute to the natural function of many 7-transmembrane-segment receptors and may be a modification common to primate immunodeficiency virus coreceptors.See also 8674119] [Full Text]" pmid="8674119"Rottman et al.(1997) showed by immunohistochemistry and flow cytometry that CCR5 is expressed by bone marrow-derived cells known to be targets for HIV-1 infection, including a subpopulation of lymphocytes and monocytes/macrophages in blood, primary and secondary lymphoid organs, and noninflamed tissues.(1998) found transient natural resistance over time of most of 128 hemophiliacs who were inoculated repeatedly with HIV-1-contaminated factor VIII (300841) concentrate from plasma during 1980 to 1985, before the development of the HIV blood test.Furthermore, and remarkably, 14 subjects remained unaffected to the time of the report, and in these subjects homozygous CCR5 mutations were found in none, but in most of them there was overproduction of beta-chemokines.This Primer by Greg Gibson helps explain why thousands of variants of small effect contribute to complex traits. (1996) cloned a human C-C chemokine receptor gene from a human genomic DNA library based on its similarity to a murine C-C chemokine receptor clone (MOP020).

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