Sentence examples for defective secretion from inspiring English sources

In cystic fibrosis, which is believed to arise as a result of mutations in this Cl−-HCO3− channel (De Braekeleer and Daigneault, 1992), defective secretion of HCO3− by enterocytes leads to defects in mucus secretion by the goblet cells, resulting in abnormally thick, aggregated, mucus (Garcia et al., 2009).

Inactivation of SREBP1c in these islets, however, failed to normalize GSIS, thereby excluding SREBP1 and triglyceride-accumulation as the main cause behind defective secretion in this model [57].

Overexpression of Rho3 also suppressed the fragmentation of vacuoles, and the accumulation of v-SNARE Syb1 in Golgi/endosomes and partially suppressed the defective secretion associated with apm1-deletion cells.

The absence or downregulation of the beta subunit may cause defective secretion of APOB-containing lipoproteins, which would then promote development of beta-lipoproteinemia, an autosomal recessive disease [122], [123].

Defective ciliary function in these compartments has been linked to defective secretion (by the epithelia of the CP) or movement (by the beating of the ependymal cilia) of cerebrospinal fluid (CSF), ultimately causing dilatation of the brain ventricular system and hydrocephalus [31] [38].

Diabetes is one of the most common metabolic disorders, characterized by defective secretion of insulin.

However, MIDY mutants with or without an odd number of cysteines [C(A7)Y or L(B11 P] were not only defective for secretion but also inhibited secretion of tagged proinsulin-WT (Fig. 4C).

ΔssaV, a mutant strain defective in secretion by the SPI-2 type three secretion system (TTSS), was used as positive control because SPI-2 encoded TTSS is essential for S. enterica to proliferate inside host macrophages [5].

This is in contrast to our findings of defective cytokine secretion, which indicates that TNF and IL6 secretion is partially dependent on the expression of OPTN but independent of its ability to bind ubiquitin in BMDMs.

Cre transgene (βAMPKdKO mouse) leads to impaired glucose tolerance and defective insulin secretion in vivo but enhanced glucose-stimulated insulin secretion from isolated islets.

We revealed impaired angiogenesis in terms of reduced branching and inhibition of proper EC migration owing to defective neural secretion in Tgfbr2-cKO, rather than defects in pericyte recruitment, endothelial cell proliferation or expression of cell junction proteins.