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Example sentences for: lte
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Tem1 is thought to be kept inactive throughout early mitosis by the two-component GTPase-activating protein complex Bub2/Bfa1 which co-localizes with Tem1 at the spindle pole body [ 10 11 ] . When the mitotic spindle penetrates the mother-daughter neck, the Tem1-bound spindle pole body is translocated into the daughter cell where a cortical pool of Lte1 is thought to activate Tem1 [ 12 13 ] . In addition to this spatial regulation, the GTPase activity of Bfa1 is thought to be inactivated through its phosphorylation by Cdc5 [ 14 ] , but it remains unknown how this process is coordinated with the presumed juxtaposition of Lte1 and Tem1 in the daughter cell.
In pre-anaphase cells, Cdc14 is confined to the nucleolus as a subunit of the RENT complex (which also contains Net1/Cfi1 and Sir2), and its phosphatase activity is inhibited by Net1 [ 8 9 10 11 ] . Damaged DNA and mis-oriented mitotic spindles delay exit from mitosis (reviewed in [ 12 ] ), but after errors have been rectified or bypassed, Lte1, Nud1, and possibly other unidentified factors [ 13 ] promote Tem1 activation.
Identified components of the MEN include Tem1 (a GTP-binding protein), Lte1 (a putative guanine nucleotide releasing factor), Nud1 (a spindle-pole-body protein), Cdc15 (a protein kinase), Dbf2/Mob1 (a protein kinase complex), Cdc5 (a Polo-like protein kinase), and Cdc14 (a protein phosphatase).
They encode the GTP-binding protein Tem1 and its putative guanine nucleotide releasing factor Lte1, the dual specificity protein phosphatase Cdc14, protein kinases Cdc5, Cdc15, and Dbf2/Dbf20, the Dbf2-binding protein Mob1 (reviewed in [ 4 ] ) and the spindle-pole-body component Nud1 [ 5 ] . Conditional-lethal temperature sensitive (ts) mutations in any of the MEN genes cause cells to arrest in late mitosis with elevated mitotic Cdk activity when shifted to the restrictive temperature.
The cysteinyl leukotrienes (CysLT), LTC, LTD, and LTE, were first shown to be essential mediators in asthma [ 29 ] . However, when the mouse leukotriene B4 receptor (m-BLTR) gene, was cloned it was shown to have significant sequence homology with chemokine receptors (CCR5 and CXCR4), co-receptors for many different HIV-1 clades [ 30 ] . Along the same lines, when cells were infected with 10 primary clinical isolates of HIV-1, leukotriene B4 receptor was primarily utilized for efficient entry into cells which were mainly of the syncytium-inducing phenotype [ 31 ] . Therefore, up-regulation of neuropeptide Y-like receptor and down-regulation of leukotriene B4 receptor in Tat expressing cells indicates a selective advantage of one class of virus (CCR5) over another (CXCR4).
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