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EC Number
Amino acid exchange
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
1.5% of wild-type activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl as substrate
no activity with (7-methoxycoumarin-4-yl)acetyl-APK-2,4-dinitrophenyl
angiotensin I cleavage activity is 21% of wild-type activity, angiotensin II cleavage activity is 71.8% of wild-type activity
the point mutation in the ACE2 ectodomain markedly attenuates shedding. The resultant ACE2-L584A mutant trafficks to the cell membrane and facilitates SARS-CoV entry into target cells
ACE2 overexpression leads to markedly increased myocyte volume, assessed in primary rabbit myocytes
construction of a soluble truncated mutant enzyme lacking the transmembrane and cytosolic domains
construction of cytoplasmic tail deletion mutants by introduction of a stop codon at position amino acid 763. Construction of chimeric proteins containing portions of human ACE2 and portions of human CD4 or human beta-defensin-2, both showing loss of domain shedding
construction of several transgenic linages with differential virological and immunological outcome of severe acute respiratory syndrome coronavirus infection in susceptible and resistant transgenic mice expressing human ACE2, overview. Transgenic lineages AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively, are both permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appears to be more intense in AC70 than in AC22 mice, especially in the brain, differential SARS-CoV-induced morbidity and mortality between AC70 and AC22 mice, overview
Results 1 - 10 of 28 > >>