Words similar to decarboxylase
Example sentences for: decarboxylase
How can you use “decarboxylase” in a sentence? Here are some example sentences to help you improve your vocabulary:
They are: two ubiquitin precursors UBA80 (clone 1) and UBA52 (clone 21), the ornithine decarboxylase antizyme (Az) (clone 15) and the proteasome β subunit HsN3 (clone 18).
For example, the complementary sequence shared between Dopa decarboxylase and CG10561 is thought to be involved in regulating the levels of these transcripts [ 45].
The cell surface expressed integrins can control this process by physically interacting with the extracellular matrix proteins and other cell surface proteins on endothelial cells lining the blood vessel wall [ 1 ] . These integrins signal adhesion and migration by communicating with several tyrosine kinases inside the cell, including the Focal Adhesion Kinase (FAK) and Src family kinases [ 1 2 ] . Src kinases control the activation of FAK, as well as the tyrosine phosphorylation of critical substrates that regulate adhesion and migration [ 3 ] . Indeed, colon cancer cells with high metastatic potential have elevated levels of Src activity or activating mutations in the Src gene [ 4 5 ] . One Src substrate that is involved in regulating an important signaling node in this process is the adaptor protein p130 cas (Cas) [ 6 7 8 9 10 ] . Cas appears to play a central role in the transformation process by several oncogenes including ras, ornithine decarboxylase (ODC), v-Src, v-crk, and Bcr-Abl, as these tumors all have elevated levels of tyrosine phosphorylated Cas [ 6 11 12 13 ] . Cells from mice that lack Cas have much reduced migration and are resistant to transformation by v-Src, while expression of Cas anti-sense RNA in cells transformed with ras, v-Src or ODC result in reversion of the transformed phenotype [ 11 14 15 ] . Furthermore, increased expression of Cas can rescue cell migration and adhesion in cells expressing the tumor suppressor PTEN, and can enhance cell migration and adhesion in normal cells, with a major role being played by the substrate domain [ 16 17 ] .
T1DM susceptibility in the NOD mouse is linked to I-A g7, the murine MHC class II gene that encodes a histidine at position 56 and a serine at position 57 in the β chain, in place of the more frequent proline 56β and aspartic acid 57β [ 3 ] . The development of diabetes is prevented in NOD.PD mice (which are NOD mice with I-A g7) that carry a β chain transgene with site-specific mutations that restore proline and aspartic acid at positions 56β and 57β, respectively [ 4 ] . Furthermore, because of the two amino acid changes in the additional (transgenic) MHC class II allele β chain in NOD.PD mice, NOD.PD mice recognize three additional peptide epitopes in the glutamic acid decarboxylase 65 (GAD65) autoantigen [ 5 ] .
Az was previously identified as a polyamine-inducible factor that binds and targets the ornithine decarboxylase (ODC) to proteasome for degradation [ 18 45 ] . Until now, ODC is the only protein known to be targeted by Az to proteasome, although the existence of additional proteins targeted by Az to proteasome has been suspected [ 20 ] . We now find two new Az interactors: Smad1, the key signal transducer of BMPs, as well as SNIP1, the nuclear repressor of CBP/p300.
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