Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.22.1 (DNase II)
 429 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nanomaterials are finding increasing use in industrial production and daily life. However, human exposure to them may cause health risks. Nano-SiO(2) was selected as a representative nanomaterial and its potential effects were investigated in terms of its interactions with cytochrome c (cyt c), deoxyribonuclease (DNase II) and hemoglobin (Hb). The interactions accorded with Langmuir isothermal adsorption; the saturation binding numbers for cyt c, DNase II and Hb were 42+/-5, 24+/-2 and 1.1+/-0.1 micromol/g nano-SiO(2) particle at pH 7.4, respectively, and the corresponding stability constants were 6.15 x 105, 1.79 x 106 and 2.6 x 107 M(-1). On the basis of the binding constants and of zeta-potential fluorescence and circular dichroism (CD) measurements and scanning electronic microscopy (SEM), it was found that the three functional proteins can bridge nano-SiO(2) particles via charge attraction and hydrogen bonding and aggregate them into coralloid forms. The interactions also changed the secondary structures of the proteins and inhibited their static and dynamic activities. It may reasonably be deduced that exposure to nano-size silicon dioxide particles e.g. as drug carriers may have an unfavorable effect on human health by inactivating functional proteins.
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PMID:Effects of nano-sized silicon dioxide on the structures and activities of three functional proteins. 2047 50

Amiloride derivatives are a class of new promising chemotherapeutic agents. A representative member of this family is the sodium-hydrogen antiporter inhibitor HMA (5-(N,N-hexamethylene amiloride), which has been demonstrated to induce cellular intracytosolic acidification and cell death through the apoptotic pathway(s). This work aims at characterizing drug response of human cancer cell lines to HMA. After a first screening revealing that HMA interferes with cancer cell survival, we focused our attention on SW613-B3 colon carcinoma cells, which are intrinsically resistant to a panel of drugs. Searching for the activation of canonical apoptosis, we found that this process was abortive, given that the final steps of this process, i.e. PARP-1 cleavage and DNA ladder, were not detectable. Thus, we addressed caspase-independent paradigms of cell death and we observed that HMA promotes the induction of the LEI/L-DNase II pathway as well as of parthanatos. Finally, we explored the possible impact of autophagy of cell response to HMA, providing the evidence that autophagy is activated in our experimental system. On the whole, our results defined the biochemical reactions triggered by HMA, and elucidated its multiple effects, thus adding further complexity to the intricate network leading to drug resistance.
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PMID:Multiple effects of the Na(+)/H (+) antiporter inhibitor HMA on cancer cells. 2399 9