Example sentences for: non-covalently

How can you use “non-covalently” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Those versions that lack the heme-binding histidine might either non-covalently interact with heme, as in the case of the SGC α-subunits, or bind some other unknown ligand.

  • In response to receptor activation, Syk becomes non-covalently associated with the BCR through tandem SH2 domains located in the amino terminal half of the protein [ 44 ] . Following engagement of the BCR, phosphorylation of specific tyrosine residues in immunoreceptor tyrosine-based activation motifs (ITAMs) found within the cytoplasmic tails of CD79a and CD79b provides docking sites for Syk localization [ 45 46 47 ] . The ability of phosphorylated ITAM peptides to selectively enhance Syk kinase activity in vitro suggests that recruitment of Syk to the receptor complex may serve to activate the kinase, in part, through allosteric changes in the structure of the Syk protein [ 44 48 49 ] . Upon activation, Syk and the receptor complex become localized in detergent-resistant cholesterol-rich membrane microdomains (lipid rafts), resulting in the segregation of the BCR complex from other membrane components [ 50 ] .

  • Though SGC α-subunits lack the histidine, the region encompassing the HNOB domain in human SGC1α has been shown to be important for functional heme binding by the dimeric enzyme [ 28 ] . Hence, in addition to covalent heme binding, HNOB domains may also interact with it non-covalently.

  • After cleavage of the DNA gate strand which becomes covalently linked to Tyr319 on Top67 (step 2), protein conformational change involving both Top67 and the ZD domain increases the distance between the covalently bound 5' phosphate and non-covalently bound 3' hydroxyl of the cleaved DNA gate strand while the passing DNA strand (T-strand) is guided through the "gate" via interaction with the ZD domain (step 3) to lead to change in linking number.

  • In immature B cells, activation through the BCR induces either a state of unresponsiveness, termed anergy, or death by apoptosis, depending on the physical nature and concentration of the antigen [ 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 ] . In some B cell lymphomas, activation through the BCR can induce cell cycle arrest and apoptosis in vitro and tumor dormancy in vivo [ 19 26 27 28 ] . The core of the multi-subunit BCR is membrane-bound immunoglobulin (mIg), which is non-covalently associated with two co-receptor molecules, CD79a (Igα) and CD79b (Igβ), products of the mb-1 and B29 genes [ 29 30 ] . The biochemical changes induced by engagement of the BCR are extensive and include an increase in tyrosine phosphorylation of several intracellular proteins, hydrolysis of membrane phospholipids, fluxes in the concentration of intracellular free Ca 2+, activation of several serine/threonine kinases including components of the MAP kinase pathway, and changes in the activities of a panel of transcription factors.


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