Exact(11)
A slight entry defect was measured in CHO cells expressing murine nectin-1 (Fig. 2).
Without EM, we cannot rule out the possibility that p85 deficient cells also have an entry defect.
As TRPC6 channel activation can partially overcome this Ca2+ entry defect, specific TRPC channel activators may be potential new drug candidates for the topical treatment of psoriasis.
However, the entry defect of ΔsipD S. Typhimurium was abolished when the SipD of either S. Typhi or S. Typhimurium was expressed (Fig. 3B and C).
The entry defect of ΔsipD S. Typhi was abolished when the SipD of S. Typhi was expressed but not when the SipD of S. Typhimurium was expressed.
As TRPC6 channel activation could partially overcome this Ca2+ entry defect in psoriasis keratinocytes, specific TRPC6 channel activators e.g. out of the phloroglucinol class may be potential new drug candidates for the topical treatment of psoriasis.
Similar(49)
However, such treatment did not affect AAV9 virions, suggesting a potential entry/post-entry defect for the mutant in different tissues.
Thus, Snf1 activation can occur in the absence of G1/G0 entry, and defects in Snf1 activation are unlikely to explain the failure of autophagy-deficient yeast to properly arrest in G1/G0 in response to nitrogen starvation.
Oxygen exposure to graphite containing Ar+-produced defects does not influence Cs clustering at the defects or Cs entry into galleries beneath the defect.
This defect in entry could be due to downregulation of SPI1 genes required for entry into non-phagocytic host cells.
None of the mutants displayed any defects in entry or colocalization with LAMP-1 (Fig. 5C), suggesting the infectious block of the cysteine mutants does not involve cell binding or intracellular trafficking.
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