Category:Team Polly Morphic

Figure 5B shows that JNK1 efficiently phosphorylates MAP and 5D shows that it is specific. At low concentrations, JNK1 is a predominant MAP2 kinase. In Figure 6A, JNK1 deficient mice displayed 3 fold lower labelling of MAP2 and in 6B MAP2 polypeptides are significantly lowered in JNK1 deficient mice. JNK1 is an important MAP2 kinase.

Figure 4 shows that inhibition of JNK1 results in shorter and more numerous dendritic processes. Figures 7 and 8 support JNK1 involvement in the development of the shape and size of the dendritic processes by pictures and analyzation of the dendrites.

Figure 2E, JNK1 deficient neurons migrate faster than wild type neurons, as 3 times as many JNK deficient cells had migrated. Figure 7E supports this, showing that JNK deficient cells migrate at a faster speed in a time lapse study. JNK1 is involved in migration of neurons.

Figure 4 shows the constriction of the visual field in individuals affected with a homozygous p.Tyr3156X mutation in EYS and a non-recordable ERG or ERG responses in a rod-cone pattern. One patient (4C) also demonstrated a photoreceptor dystrophy.

Figure 2B: At high intensity light stimulus, the a-wave and sensitivity of the scotopic GC2 (GUCY2F) -/- mouse were slightly reduced compared to the WT.

Figure 4,5. Fig. 4 shows the absence of isomerase activity activity in pRPE65-transerase 293T-RC cell homogenates using atROL as substrate and the presence of activity in the same cells using atRP as substrate. pRPE65-transfected likes do show isomerase activity.

Figure 2 shows the analysis of GC1 protein level expression in normal and rd/rd (retinal dystrophy affected)chicken retina using western blot probed with anti-retGC pAb GC2.

Figure 2C shows the failure of MII-deficient cells to give rise to hematopoietic colonies. Figure 2 A and B shows the normal development of cells for MII and MII-deficient cells, indicating normal differentiation. Thus, MII-deficient cells develop normally until hematopoietic differentiation. The lack of differentiation results in a failure to develop a hematopoietic center in the body.

Table 2 and Figure 3 show that the amplitudes of the 30Hz flicker response were significantly reduced in the dogs homozygous for the RPGRIP1 mutation compared to the control group.

Figure 3: Ccdc66 -/- mouse at 3 months revealed a reduced a-wave amplitude under scotopic conditions and a reduced b-wave amplitude under photopic conditions on a background intensity of 25 cd/m^2.

Figure 3: Establishes ADAM9 mutation in dogs affected with crd3 in this study. Figure 4: ADAM9 mutation is crd3 affected dogs causes a frame shift mutation resulting in a premature stop codon at base 6 of exon 17. Figure 1:By 15 months of age ERG dysfunction is detected as reduced 30Hz flicker cone responses in dogs affected with crd3 due to ADAM9 mutation, and at later ages by continued deterioration of cone and rod responses in these affected dogs.

Figure 4: Average dark adapted a- and b- ERG wave amplitudes from mutant PDE6A puppies peaked at three weeks of age and were significantly smaller than control puppies of the same age. Mean light adapted a-wave amplitudes of affected dogs were lower than normal dogs at 3 weeks of age and decreased with increasing age.