Purification and properties of xanthine dehydrogenase from Pseudomonas acidovorans.

Xanthine dehydrogenase (EC 1.2.1.37) from Pseudomonas acidovorans has been purified to near homogeneity (approx. 65-fold). The enzyme has a molecular weight of about 275 000. Electrophoresis in gels containing sodium dodecyl sulphate showed the presence of two types of subunit with molecular weights of about 81 000 and 63 000. Thus the intact molecule probably contains two of each type of subunit. Xanthine and hypoxanthine are good substrates, and NAD+ is an effective electron acceptor. With xanthine and NAD+ as substrates the purified enzyme has a specific activity of about 20 mumol NADH formed/min per mg protein. Michaelis constants for xanthine and NAD+ are 0.07 and 0.12 mM, respectively, and for hypoxanthine and NAD+ 0.29 and 0.16 mM, respectively.     

The P2X7 receptor antagonist JNJ-47965567 administered thrice weekly from disease onset does not alter progression of amyotrophic lateral sclerosis in SOD1G93A mice

Purinergic Signalling - The ATP-gated P2X7 ion channel has emerging roles in amyotrophic lateral sclerosis (ALS) progression. Pharmacological blockade of P2X7 with Brilliant Blue G can ameliorate...     

不同生长调节剂及基质对越南粉苞茉莉扦插生根的影响

为探索越南粉苞茉莉(Jasminum dichotomum)扦插生根的影响因素,建立扦插繁育技术体系,以1年生越南粉苞茉莉枝条为插穗,采用L16(44)正交试验,探讨生长调节剂种类及其浓度、处理时间、基质种类对越南粉苞茉莉茎段扦插生根的影响,利用排队评分法和公式评分法对正交试验进行分析。结果表明,A2B3C3D2为试验的最优处理组合,即将插穗在250 mg·L-1 IBA和500 mg·L-1 NAA混合药剂中浸泡20 min后扦插于沙子上。     

Activation of acid growth in germinating horse chestnut seeds

The validity of the acid-growth hypothesis is proved for the case of cell elongation initiation in germinating seeds of horse chestnut (Aesculus hippocastanum L.), the embryo axes of which are known to extend during the first stages of germination only by cell elongation. During seed imbibition, H⁺-ion excretion was firstly low; it increased several times prior to radicle emergence and was maintained at a high level during growth initiation and further cell elongation. Cell wall acidification and radicle emergence were enhanced in the presence of 0.02 mM fusicoccin, thus indicating the involvement of the plasma membrane H⁺-ATPase in the execution of acid growth. The presence of this enzyme and its activator (14-3-3 protein) in microsomal fractions obtained from radicles and hypocotyls of the embryo axes during and after initiation of cell elongation was demonstrated immunochemically. It is supposed that the initiation of cell elongation at early germination occurs via the activation of the plasma membrane H⁺-ATPase and results in the acidification of cell walls, leading to their higher extensibility, in accordance with the hypothesis of acid growth.     

Silencing of cytosolic NADP+-dependent isocitrate dehydrogenase by small interfering RNA enhances the sensitivity of HeLa cells toward staurosporine

Staurosporine induces the production of reactive oxygen species, which play an important causative role in apoptotic cell death. Recently, it was demonstrated that the control of cellular redox balance and the defense against oxidative damage is one of the primary functions of cytosolic NADP⁺-dependent isocitrate dehydrogenase (IDPc) by supplying NADPH for antioxidant systems. The present report shows that silencing of IDPc expression in HeLa cells greatly enhances apoptosis induced by staurosporine. Transfection of HeLa cells with an IDPc small interfering RNA (siRNA) markedly decreased activity of IDPc, enhancing the susceptibility of staurosporine-induced apoptosis reflected by DNA fragmentation, cellular redox status and the modulation of apoptotic marker proteins. These results indicate that IDPc may play an important role in regulating the apoptosis induced by staurosporine and the sensitizing effect of IDPc siRNA on the apoptotic cell death of HeLa cells offers the possibility of developing a modifier of cancer chemotherapy.     

Latency Locus Complements MicroRNA 155 Deficiency In Vivo

MicroRNA-155 (miR-155) is expressed in many cancers. It also executes evolutionary conserved functions in normal B cell development. We show that the Kaposi''s sarcoma-associated herpesvirus (KSHV) latency locus, which contains an ortholog of miR-155, miR-K12-11, complements B cell deficiencies in miR-155 knockout mice. Germinal center (GC) formation was rescued in spleen, lymph node, and Peyer''s patches. Immunoglobulin levels were restored. This demonstrates that KSHV can complement the normal, physiological function of miR-155.