knock out mice การใช้

• This hypothesis has also been questioned after knock out mice were created.
• Previous studies showed that MAP1LC3B knock out mice develop normally, possibly due to a then unknown compensatory mechanism.
• Surprisingly, pax5 conditional knock out mice allowed peripheral mature B cells to de-differentiate to early bone marrow progenitors.
• Also ADAR1 knock out mice show increase in apoptosis which indicates editing may be involved in regulation of the cellular process.
• In Nkx2-5 knock out mice, cardiac development halts at the linear heart tube stage and looping morphogenesis disrupted.
• The phenotype of knock out mice demonstrates that pdgfrb is essential for vascular development, and that pdgfb is responsible for activating PDGFR? during embryogenesis.
• In this way, in Krox-20 double knock out mice, it has been recorded that hindbrain segmentation is affected as well as myelination of Schwann cell associated axons.
• Antibody targeting of TIRC7 reveals significant prevention of inflammation in variety of animal models e . g . memory cell subset and reduction of CTLA4 expression observed in TIRC7 knock out mice.
• APLP2 / APP double knock out mice and APLP2 / APLP1 double knock out mice each show a lethal phenotype ( postnatal day 1 ), whereas APLP1 / APP double knock out mice are apparently normal, demonstrating the importance of the APLP2 protein.
• APLP2 / APP double knock out mice and APLP2 / APLP1 double knock out mice each show a lethal phenotype ( postnatal day 1 ), whereas APLP1 / APP double knock out mice are apparently normal, demonstrating the importance of the APLP2 protein.
• APLP2 / APP double knock out mice and APLP2 / APLP1 double knock out mice each show a lethal phenotype ( postnatal day 1 ), whereas APLP1 / APP double knock out mice are apparently normal, demonstrating the importance of the APLP2 protein.
• The C site has been shown to be mainly edited by ADAR2 but in presence of upregulated expression of ADAR1, there was an increase in editing of this site and the enzymes presence can also result in limited editing in ADAR 2 knock out mice.
• Mouse model studies using the IL-17RA knock out mice and the IL-17A knock out mice with the murine adapted influenza strain ( PR8 ) as well as the 2009 pandemic H1N1 stain [ 93 ] both support that IL-17A plays a detrimental role in mediating the acute lung injury.
• Mouse model studies using the IL-17RA knock out mice and the IL-17A knock out mice with the murine adapted influenza strain ( PR8 ) as well as the 2009 pandemic H1N1 stain [ 93 ] both support that IL-17A plays a detrimental role in mediating the acute lung injury.
• INOS  " /  " mice also show decreased immunity, indicating a direct role of CD4 +-stimulated iNOS production in protection against tumours . ( Hung et al ., 1998 ) Similar results have been seen in knock out mice deficient in gp91phox, a protein involved in the production ROIs ( Reactive Oxygen Intermediates ) which are also an important weapon utilized by macrophages to elicit cell death.
• One study of APOE knock out mice showed cold exposure could promote atherosclerotic plaque growth and instability when study mice were subjected to sustained low temperatures of 4 癈 for 8 weeks, which may cause a stress condition that shows rapid forced change rather than a safe acclimatisation that can be used to understand the potential in adult humans during modest reductions of ambient temperature by just 5 to 10 癈 . Furthermore, several newer studies have documented the substantial benefits of cold exposure in multiple species including humans, for example researchers concluded that " activation of BAT is a powerful therapeutic avenue to ameliorate hyperlipidaemia and protect from atherosclerosis " and that brown fat activation reduces plasma triglyceride and cholesterol levels and attenuates diet-induced atherosclerosis development.