The phrase "a marked defect" is correct and usable in written English.
It can be used to describe a noticeable or significant flaw in an object, process, or system.
Example: "The inspection revealed a marked defect in the product's design that could lead to safety issues."
Alternatives: "a significant flaw" or "a noticeable imperfection."
Consistent with the temperature-dependent cell morphology changes in the pmt mutants, both pmt1A and pmt4A strains displayed a marked defect in growth at elevated temperatures (Figure 5).
In support of this idea, contraction of circumferential actin belt in lining epithelial cells is critical for closure of the neural tube [31], and Syt-null mouse embryos have a marked defect in neural tube closure (Kimura, 2009).
The defects in Vav1-deficient thymic development, including a marked defect in DN3-DN4 transition, were completely reversed by Cbl inactivation, accompanied by enhanced phosphorylation of PLC-γ1 and ERKs in response to pre-TCR/TCR cross-linking of Vav1-/-Cbl-/ DP thymocytes.
Anaemia is microcytic and characterised by a marked defect in iron supply for erythropoiesis [ 4].
As described earlier, a marked defect was observed in the class-switched isotypes in the ICOS /– mice (Fig. 1).
There is a marked defect in neutrophil migration into the infectious focus during severe sepsis, which is associated with the severity of disease.
These data characterize a novel group of subjects with type 1 diabetes manifested solely by hyperglycemia following an oral glucose load in whom islet function is normal at euglycemia, but who have marked defects in both alpha- and beta-cell secretion at hyperglycemia.
The NF-κB signaling pathway was suspected to be crucially involved in the development of naturally occurring Treg cells, because mice lacking molecules of proximal TCR signaling leading to NF-κB activation, such as PCKθ, Bcl10, or CARMA1, show marked defects in the thymic generation of Treg cells [48], [49], [50], [51].
However, the axonal arborizations of mutant PNs in the protocerebrum manifested marked defects.
Evidence has emerged that TLR4 defective mice do not develop LV dysfunction after LPS stimulation whereas wild type mice developed marked defects in LV contraction and relaxation [ 25].
Thus, NON mice have a marked secretory defect, which is corrected to a significant degree by amiloride derivatives.
