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As expected, delivery of OVA protein into RMA-S, a cell line with a deficiency in MHC class I antigen processing due to a TAP defect, failed to present the SIINFEKL epitope to B3Z.
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The T2 line is a TAP-defect cell line derived from the human T cell leukemia/B cell LCL hybrid 174 (Salter and Cresswell, 1986).
Instead, it is likely that the tap habituation defect in rpm-1 mutants is a consequence of the developmental abnormalities in these animals.
A pilot screen for tap habituation defects revealed several mutants with abnormal habituation, demonstrating how this high-throughput method will expand the genome phenome matrix.
Previous work has shown that each of these types of neurons that make up the tap circuit have developmental defects in rpm-1 mutants.
Moreover, defects in overall TAP expression (defined as partial or total loss of either or both of the TAP subunits) were significantly associated with HLA class I down-regulation (P < 0.001).
We found that rpm-1 mutants had slight hypersensitivity to the initial tap stimulus, but extremely strong defects in habituation to tap.
To determine whether the secretion defect of the tap-1 mutant is specific for TseL or affects T6SS-mediated secretion universally, we analyzed Hcp secretion in V52∆ tap-1, as Hcp secretion is the hallmark of a functional secretion system.
Showers and baths are associated with exposure to WDBPs [ 10, 11], and epidemiological studies have inconsistently reported associations between maternal exposure via tap water and risk for birth defects (reviewed in [ 9, 12]).
The general hypothesis was that exposure to disinfection by-products through tap water increases the risk of birth defects.
These defects suggest that Tej and Tap together could support primary processing, probably by engaging Aub and/or Piwi, and a more robust ping-pong amplification cycle for piRNA amplification.
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