Exact(1)
Also these enzymes can sometimes be deficient completely and not synthesized by the cell.
Similar(59)
Introduction of PrP on the PrPKO background reverses the iron deficient phenotype completely, indicating that PrP is an integral component of the iron homeostatic machinery that feeds into the major pathways of iron uptake and transport.
Prox1-deficient embryos completely lack lymphatic development due to a failure in LECs specification (Wigle et al, 2002).
Vegfr3/ flt4-deficient zebrafish completely lack lymphatic vessels but show no major defects in blood vessel growth [ 9].
Indeed, the complex deficiency of the Irgm1-deficient mouse is completely reversed in the Irgm1/Irgm3 double-deficient mouse (Henry et al., 2009a), showing that neither the presence of Irgm1 nor of Irgm3 is in fact required for resistance to the 'Irgm1-dependent' organisms such as Salmonella or Mycobacteria.
Minor points In the Introduction the Authors report the classical classification of PNH cells as Type III (completely deficient in GPI anchored proteins), Type II (partially deficient) and Type I (normal display of GPI-linked proteins).
The BT mice differ from the Ar-KO mice in that the Ar-KO mice are completely deficient in AR whereas the BT mice are deficient in AR in all tissues, including most parts of the kidney, except the medullary collecting tubule epithelial cells that carry the knockin transgene.
Consistent with the result in Malt1 KO MEF cells, both CARMA3-deficient and BCL10-deficient cells were completely defective for NF-κB activation upon doxorubicin treatment.
We used mice with T cell-specific deletion of Stim1 and Stim2 genes, which have severely reduced SOCE (Stim1-deficient mice) or completely abolished SOCE (Stim1/Stim2-deficient mice).
PNH cells can be completely deficient in GPI anchored proteins (Type III) or partially deficient due to residual activity of the PIGA protein (Type II), while PNH Type I cells express GPI-linked proteins normally.
Recently, we reported in vivo studies of tankyrase 2 function using mice genetically engineered to be completely deficient in TANK2 or to express a PARP-deficient TANK2 mutation.
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