Null mouse

B2 knockout embryos subjected to salt stress in utero show suppressed renin expression and an abnormal kidney phenotype and develop early postnatal hypertension. Consistently, although basal bradykinin formation is defective tissue kallikrein-null mice have normal blood pressure however suffer from cardiovascular abnormalities. However suggesting a function of kinin signaling during development. 

Development of MMP null mice carrying specific MMP deletions has provided an opportunity to explore the role of MMPs in normal development as well as in such diverse conditions and diseases as skeletal dysplasias, coronary artery and heart disease, arthritis, cancer, and brain disorders. 

CIA in IFNyR null mice DBA/1 mice AMD3100 (JM3100) i Inhibition of monocyte migration to CXCL12a. Reduction of DTH response to collagen type II. 208... 

Quinones MP, Ahuja SK, Jimenez F, et al. Experimental arthritis in CC chemokine receptor 2-null mice closely mimics severe human rheumatoid arthritis. J Clin Invest 2004 113(6) 856-866. 

Doi M Yujnovsky I., Hirayama J. et al. (2006). Impaired light masking in dopamine receptor-null mice. Nat. Neurosci. 9, 732-4. 

The orexin receptor null mice OXjRW, OX2R, and OXjR J ox2R G... 

As predicted, MCH l orexin mice displayed an intermediate body weight phenotype, indicating independent and opposing neuromodulatory actions of MCH and orexin on metabolism. Surprisingly, however, rather than expressing an attenuated narcoleptic phenotype, MCHr orexin l mice exhibited more severe behavioral state instability during the active phase. When compared with orexin mice, the double null mice had about twice as many cataplectic episodes (Fig. 15.7A), they were less able to maintain wakefulness, and... 

Willie, J. T., Chemelli, R. M., Sinton, C. M. et at (2003). Distinct narcolepsy syndromes in Orexin receptor-2 and Orexin null mice molecular genetic dissection of Non-REM and REM sleep regulatory processes. Neuron, 38, 715-30. 

Cole AR et al. Proteomic analysis of colonic crypts from normal, multiple intestinal neoplasia and p53-null mice a comparison with colonic polyps. Electrophoresis 2000 21 1772-1781. 

Miyashiro, K. Y., Beckel-Mitchener, A., Purk, T. P., Becker, K. G., Barret, T., Liu, L., Carbonetto, S., Weiler, I. J., Greenough, W. T., andEberwine, J. (2003). RNA cargoes associating with FMRP reveal deficits in cellular functioning in Fmrl null mice. Neuron 37, 417-431. 

Myelin basic protein. In PNS myelin, MBP varies from approximately 5% to 18% of total protein, in contrast to the CNS, where it is close to 30% [ 1 ]. In rodents, the same four 21,18.5,17 and 14kDa MBPs found in the CNS are present in the PNS. In adult rodents, the 14kDa MBP is the most prominent component and is termed Pr in the PNS nomenclature. The 18.5 kDa component is present and is often referred to as the P, protein in the nomenclature of peripheral myelin proteins. Another species-specific variation in human PNS is that the major basic protein is not the 18.5 kDa isoform that is most prominent in the CNS but rather a form of about 17 kDa. It appears that MBP does not play as critical a role in myelin structure in the PNS as it does in the CNS. For example, the shiverer mutant mouse, which expresses no MBP (Table 4-2), has a greatly reduced amount of CNS myelin, with no compaction of the major dense line. By contrast, shiverer PNS has essentially normal myelin,both in amount and structure, despite the absence of MBP. This CNS/PNS difference in the role of MBP is probably because the cytoplasmic domain of P0 has an important role in stabilizing the major dense line of PNS myelin. Animals doubly deficient for P0 and MBP have a more severe defect in compaction of the PNS major dense line than P0-null mice, which indicates that both proteins contribute to compaction of the cytoplasmic surfaces in PNS myelin [23],... 

It is noteworthy that the axonal degeneration that occurs in the PNS of MAG-null mice is not observed in the CNS, possibly because other CNS myelin proteins enhance axonal stability. These could include PLP and/or CNP, both of which are needed for axonal stability in the CNS where they are present in much higher concentration. In summary, it appears that the most important function of MAG in the PNS is transmitting a signal from Schwann cells to axons that is needed for the stability of myelinated axons, whereas its principal function in the CNS is to transmit a signal in the reverse direction that promotes efficient myelination and oligodendrocyte vitality. 

Arikawa-Hirasawa, E., Rossi, S. G., Rotundo, R. L. and Yamada, Y. Absence of acetylcholinesterase at the neuromuscular junctions of perlecan-null mice. Nat. Neurosci. 5, 119-123, 2002. 

Laurent, V., Jaubert-Miazza, L., Desjardins, R., Day, R. and Lindberg, I. Biosynthesis of proopiomelanocortin-derived peptides in prohormone convertase 2 and 7B2 null mice. Endocrinology 145 519-528, 2004. 

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