Exact(7)
Screening of the Tn917 transposon library identified two further clones with defective survival.
In this study, we demonstrate that ICOS-deficient EM CD4 T cells have defective survival, and in ICOS-deficient patients, CVID is not usually diagnosed until adulthood [37], a point at which the population of naïve CD4 cells is declining and the body begins to depend more on memory cells [40].
Then, we have disclosed that defective survival leads to defective generation of central memory T cells in the absence of Smad4 due to aberrant transcriptional programs.
It was reported that the lack of proliferation of FADD−/− T lymphocytes results from defective survival rather than defective activation and cell cycle progression.
Although the exact signaling pathway leading to FADD-dependent T-cell proliferation is presently unclear, it was shown recently that the lack of proliferation of FADD−/− T lymphocytes results from defective survival rather than defective activation and cell cycle progression.
Spinal muscular atrophy (SMA) is a hereditary neuromuscular disease of lower motor neurons that is caused by a defective "survival motor neuron" (SMN) protein that is mainly associated with proximal progressive muscle weakness and atrophy.
Similar(53)
A screen for additional mutants of SH1000 that were defective for survival in the presence of linoleic acid identified several Tn917 transposants from a 5,000 clone library of mutants.
C. jejuni Δppk2 mutant was significantly (P≤0.01 or 0.05) defective in survival under osmotic stress both in liquid culture and on solid medium compared to WT strain (Figure 3B and 3C).
When using an fkpA mutant that is defective in survival and replication in human macrophages, pathogenicity was strongly attenuated in the zebrafish model.
Defective neuronal survival occurred in our Nrp1-null mutants on the JF1 background in the absence of obvious vomeronasal axon defects (see Fig. S1 in the supplementary material).
A similar gastrulation-defective phenotype and cell survival defect was obtained by injecting embryos with a MASO that targeted the translation initiation codon of SpPKC1 mRNA.
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