Sentences with phrase «ldlr null mice»

Their embryos had more profound defects than were seen in the Esrp1 - null mice, including craniofacial and forelimb defects, and the complete absence of lungs and salivary glands — two organs made up largely of epithelial cells.

Analysis of the neurons showed that the J20 / caspase -2 null mice had a higher density of dendritic spines than the J20 mice.

«The J20 / caspase -2 null mice showed the same dendritic spine density and morphology as the normal mice — as opposed to the deficits in the J20 mice,» said co-lead author Julio Pozueta, PhD.

At 14 months, however, the J20 / caspase -2 null mice did significantly better in the water maze test than the J20 mice and similarly to the normal mice.

To test this hypothesis, the researchers crossed J20 transgenic mice (a common mouse model of Alzheimer's) with caspase - 2 null mice (mice that lack caspase - 2).

These results suggest that the additional muscle mass induced by follistatin in Mstn null mice results from inhibition of additional ligands that act predominantly to regulate muscle fiber growth.

Additionally, they examine MMTV - PyMT control or POSTN null mice to test the effect of POSTN on primary tumor growth and metastasis (Figures 3A, 3B, and S13; Malanchi et al., 2012).

The observation of reduced calsequestrin in the muscles of IL - 15Rα — KO mice is interesting inasmuch as calsequestrin concentrations are reported to be higher in fast muscles (52) and fast muscles from calsequestrin - 1 — null mice display contractile characteristics similar to those of slow muscles, including longer contraction times and half - relaxation times (ν RTs)(53).

In order to determine whether this effect of follistatin results solely from inhibition of myostatin activity, I analyzed the effect of this transgene in myostatin - null mice.

Next generation sequencing of small RNA confirmed global suppression of miRNA and endogenous siRNA synthesis in ADAR1 - null mouse embryos.

Chen, X, Su, Y, Fingleton, B, Acuff, H, Matrisian, LM, Zent, R, Pozzi, A. Orthotopic models of lung cancer to follow primary and metastatic NSCLC growth in integrin α1 - null mice.

The p21 - null mice also developed epithelial tumors (Table 2) ⇓.

Survival of p21 - null mice.

This phenotype is reminiscent of the rich spectrum of spontaneous tumors developed by p53 - null and by p19ARF - null mice (36, 37, 38, 42, 43), albeit with a longer latency.

When the survival curve of males and females were plotted independently, the reduction in viability of p21 - null mice was more pronounced for females than for males (Fig. 1) ⇓.

We have considered the possibility that radiation could directly result in more apoptosis in the thymus of p21 - null mice; however, quantitation of sub -(G0 / G1) thymocytes after acute irradiation (10 Gy; and analysis 3 h after irradiation) has not supported this idea (data not shown).

Indeed, other investigators have reported previously (32) that the radiation - toxicity syndrome is more severe in p21 - deficient mice than in wild - type mice, and it is associated to an enhanced apoptotic response of the intestine in p21 - null mice.

Finally, there are contradictory results concerning the susceptibility of p21 - null mice to chemically induced carcinogenesis of the skin (33, 34).

We conclude that thymic lymphomas in p21 - null mice have a significantly higher level of apoptosis compared with that in wild - type mice.

We have also examined the constitutive levels of apoptosis in the thymic lymphomas developed in p21 - null mice and in wild - type mice after irradiation (Fig. 4) ⇓.

In this study, we have addressed the role of p21 in tumor suppression by directly assessing the susceptibility of p21 - null mice to spontaneous tumors and also to radiation - induced tumors.

As it was the case among irradiated wild - type mice, the predominant tumors induced by radiation in p21 - null mice were T - cell lymphomas (Table 3) ⇓.

Histology of spontaneous tumors developed by p21 - null mice.

We have carried out a detailed histopathological analysis of all of the tumors spontaneously developed by p21 - null mice (n = 65; Table 2 ⇓).

Interestingly, p21 - deficient mice did not develop T - cell lymphomas, which is one of the most common tumor types in p53 - null mice (36, 37, 38).

On the contrary, p21 deficiency delays the onset of radiation - induced T - cell lymphomas, which is in line with the delay in the appearance of spontaneous T - cell lymphomas produced by p21 deficiency in ATM - null mice (32).

Radiation - induced thymic lymphomas in p21 - null mice exhibit increased levels of constitutive apoptosis.

In support of the relevant role of p21 in mediating p53 - dependent cell - cycle arrest, cells derived from p21 - null mice arrest proliferation inefficiently after p53 activation (8, 9, 10).

Regarding p21 - null mice, it was originally reported (9) that they are tumor - free at least until 7 months of age.

For comparison, we have also followed in parallel a colony of 30 wild - type mice of the same genetic background as the p21 - null mice (i.e., C57BL6 / 129Sv 50:50).

NeuroD - null mice are deaf due to a severe loss of the inner ear sensory neurons during development.

It is interesting to note that p21 - deficient mice did not develop T - cell lymphomas, which is one of the most common tumor types in p53 - null and p19ARF - null mice (36, 37, 38, 42, 43).

The development of spontaneous tumors in p21 - null mice is in contrast to Bax - deficient mice, which do not develop tumors even after 2 years of age (44).

The second most common tumor type in p21 - null mice was of vascular origin (22 %; Table 2 ⇓).

In turn, tumour experiments in pericyte Tie2 null mice resulted in a sustained pro-angiogenic tumour vessel phenotype with strongly enhanced tumour growth.

Analysis of Sema3B null mice showed they were viable, fertile, and displayed no overt pathological abnormalities, suggesting an inherent correction mechanism or level of redundancy between the class 3 semaphorins.

Called immunodeficient IL2 receptor gamma (IL2rl) null mice, these animals lack the IL2ry receptor that humans also have as part of a functional immune system.

Rassf1A null mice were viable and fertile and displayed no pathological abnormalities.

Similarly, genetic silencing of Keap1 is insufficient to maximally activate HMOX1 gene expression in Keap1 null mice [52].

Analysis of transcriptomes in tumour tissues from wild - type mice and Slc6a14 - null mice indicated no compensatory changes in the expression of any other amino acid transporter mRNA.

Furthermore, TP63 has been implicated in human NSCL / P [44], and null mice recapitulate the human orofacial clefting phenotypes [45].

Interestingly, our in - depth analysis of the developmental defects in Boule null mice revealed a novel requirement in spermatid differentiation [61].

The previously established function of Boule in meiotic progression in both Drosophila and nematodes [39], [40] may also be conserved in mice, despite the lack of a similar meiotic defect in Boule null mice [61].

Results: We demonstrate that Ad - B2 (− / −) mice display early onset lipodystrophy, in common with congenital Bscl2 null mice and CGL2 patients.

While very high fat diets (i.e. 60 kcal % fat) are capable of inducing some atherosclerosis, the addition of cholesterol to such diets promotes more atherosclerosis in LDLr null mice (46).

Retina Restored and Brain Abnormalities Ameliorated by Single - Copy Knock - In of Human NR2E1 in Null Mice.

By contrast, Pou5f1 - null mouse embryos maintained the expression of orthologous genes, and blastocyst development was established, but maintenance was compromised.

The use of Western - type diets with added cholesterol (0.15 % - 1.25 % w / w) which are cholic acid free can induce significant atherosclerotic lesions after 12 weeks in LDLr null mice (38 - 40).

Not exact matches

Homozygous mice carrying a null mutation for the DARPP - 32 gene exhibited minimal levels of P - facilitated sexual receptivity when compared to their wild - type littermates.

C57BL / 10ScCr mice are homozygous for a null mutation of Tlr4.