Words similar to non-lymphoid
Example sentences for: non-lymphoid
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In comparison to the two general alternative mechanisms utilized by known transforming viruses to promote cell-cycle progression, namely, by activating or bypassing endogenous D-type cyclins (herein, referred to as "cyclin D"), it has not been established whether HIV-1 gene products trigger either cyclin D-dependent or cyclin D-independent proliferation in non-lymphoid tissues [ 15 ] . In infected renal epithelium, HIV-1 could disrupt the inhibitory binding of pRb to E2F independent of endogenous cyclin D, analogous to transforming viral mechanisms that bypass and down-regulate endogenous cyclin D, such as SV-40 T antigen binding to pRb [ 16 ] , HHV-8 v -cyclin binding to and activating cyclin-dependent kinase-6 (CDK) [ 17 ] , and activation of cyclin E by EBV-induced c -myc [ 18 ] . Alternatively, HIV-1 could activate cyclin D-dependent proliferation, as exemplified by RSV v -src-mediated signaling [ 19 ] . In most tissues, the selective activation of these cell-cycle pathways is readily discernable.
hCARΔcyt was not detected in non-lymphoid tissues nor on lymphocytes from non-transgenic littermate controls (data not shown).
Our finding that KRC binds to the RSS as well as the κB motif may also provide a link between transcription and recombination in the context of the accessibility model [ 58 59 ] . Enhancer or promoter elements are important for the recombination process in cell lines and animal models [ 60 ] . Similarly, expression of transcription factors, in conjunction with the recombination activating genes, has been shown to induce V(D)J recombination in non-lymphoid tissues by rendering RSS accessible to the recombinase [ 61 ] . The κB motif, first found in the Igκ light chain [ 62 ] , and later in the TCR β2 locus [ 31 ] , has been shown to promote V(D)J recombination by modulating locus accessibility [ 63 ] . In addition to influencing recombination by binding of RSS, KRC binding of the κB motif may modulate accessibility and transcription of target loci.
Proliferation and dedifferentiation of HIV-1 infected renal epithelium is singularly unique compared to the effects of HIV-1 infection in other non-lymphoid tissues.
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