Sentence examples for mouse mutants lacking from inspiring English sources

Here we show that mouse mutants lacking either SLIT2 or its receptor ROBO2, molecules known primarily for their function in axon guidance and cell migration, develop supernumerary ureteric buds that remain inappropriately connected to the nephric duct, and that the SLIT2/ROBO2 signal is transduced in the nephrogenic mesenchyme.

In this study, we characterize the circadian system of mouse mutants lacking functional Sharp-1 and/or Sharp-2 genes.

Covalent modification of proteins by SUMO is an essential process in mammals, as evidenced by the embryonic lethality of mouse mutants lacking the SUMO conjugating enzyme, Ubc9 [1].

Consistent with this, all mouse mutants lacking otoconia (such as tilted, head slant, and head tilt mice) have severe balance deficits [20], [21], [22], [23].

To this end, the analysis of conditional mouse mutants lacking CB1 receptors on different subtypes of neurons subjected to the kainic acid (KA -induced seizures revealed that CB1 receptors on hippocampal glutamatergic but not GABAergic neurons are required for protection against excitotoxic seizures [10].

Furthermore, mouse mutants lacking either the β2 or Ca v) 1.4 α1-channelannel subunits are characterized by an abnormal or absent ERG b-wave, and for the Ca v) 1.4 α1-channelannel subunit mutant, there is a loss of synaptic ribbons in the rod spherules [78] [81].

A mouse mutant lacking CaBP4, a calmodulin-like Ca2+ binding protein that interacts with Ca v) 1.4 channelsnnels, also shows defects in the ERG b-wave and reduction of the number of synaptic ribbons [82].

All of the above and more have been elegantly described by Bahloul et al through the use of a conditional mouse mutant lacking vezatin, specifically in the inner ear.

Thus, 30 E- and P-selectin-deficient scid mice homozygous mutants lacking E- and P-selectin expression and 29 scid mice homozygous wild types for E- and P-selectin as controls were included in this study.

However, it is unlikely that a defect in SCP causes lethality in GPR126LacZ mice, as other mutants lacking SCP develop to term [25].

In contrast, the deactivation kinetics of Opn4.1 and Opn4xa are similar to the mouse melanopsin mutant lacking all phosphorylatable amino acids in the carboxy-tail region.