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Endothelin 1 action on isolated rat stomach and the role of calcium ions in ET 1 induced depolarization of smooth muscle cells BC3H1. 内皮素1对离体大鼠胃的作用及钙离子在内皮素1诱导平滑肌细胞BC3H1去极化中的作用。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204422
N Hukovic, R Hadziselimovic

Endothelins; (ET1, ET2 and ET3) are a family of peptides which acts on different smooth muscle preparations inducing a slow long lasting contraction. We investigated the effects of ET 1 modulatory action on adrenergic, cholinergic and serotoninergic transmission on an isolated mouse's stomach with gastric nerves. The endothelin 1 stimulation of the mouse stomach tone was abolished by the specific serotonin antagonist methizergid. This study suggests that endothelin 1 plays a role in the regulation of nonvascular smooth muscle tone. The endothelin effect was dependent on free intracellular Ca++ which can be recruited from an extracellular solution as well as from intracellular stores. Complete reduction of Ca++ from the extracellular solution with a simultaneous depletion of calcium stores abolished endothelin 1 depolarization of BC3H1 cells.

内皮素;(ET1, ET2和ET3)是一个肽家族,作用于不同的平滑肌制剂,诱导缓慢持久的收缩。我们研究了ET 1在离体胃神经小鼠胃中对肾上腺素能、胆碱能和血清素能传递的调节作用。特异性5 -羟色胺拮抗剂甲硫肼可消除内皮素1对小鼠胃张力的刺激。本研究提示内皮素1在非血管平滑肌张力的调节中起作用。内皮素的作用依赖于游离的细胞内钙离子,钙离子可以从细胞外溶液和细胞内储存中获得。细胞外溶液中Ca++的完全还原与钙储存的同时耗尽可消除BC3H1细胞的内皮素1去极化。
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引用次数: 5
The effect of heparin and pentosan polysulfate on the thermal stability of yeast alcohol dehydrogenase. 肝素和聚硫酸戊聚糖对酵母醇脱氢酶热稳定性的影响。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204432
H Paulíková, M Molnárová, D Podhradský

Heparin and pentosan polysulfate as organic polyanions inhibit yeast alcohol dehydrogenase (YADH). The aim of this study was to determine the effect of heparin and pentosan polysulfate on the thermostability of alcohol dehydrogenase. Spectral and kinetic analyses showed that these compounds increase the thermal stability of the enzyme and eliminate entirely thermal aggregation. The thermostabilizing effect of unfractionated heparin and pentosan polysulfate was accelerated in the presence of NAD+. The addition of NAD+ (11 microM) to the incubation medium decreased the inhibition of the YADH activity in the presence of pentosan polysulfate (1.32 microM). Moreover, 38% of the residual activity of YADH was found after a 5-min incubation at 70 degrees C. These findings indicate that heparinoids not only modulate the enzyme activity but also can prevent the protein's thermal denaturation.

肝素和聚硫酸戊聚糖作为有机多阴离子抑制酵母醇脱氢酶(YADH)。本研究的目的是确定肝素和聚硫酸戊聚糖对乙醇脱氢酶热稳定性的影响。光谱和动力学分析表明,这些化合物增加了酶的热稳定性,完全消除了热聚集。在NAD+的存在下,未分级的肝素和聚硫酸戊聚糖的热稳定作用加快。在培养液中添加NAD+(11微米)可降低聚硫酸戊聚糖(1.32微米)对YADH活性的抑制作用。在70℃下孵育5 min后,发现YADH的残余活性为38%,这表明肝素类物质不仅可以调节酶的活性,还可以防止蛋白质的热变性。
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引用次数: 9
Effect of chronic alcohol ingestion on buccal mucosal expression of bFGF and Cdk2 during ulcer healing. 慢性酒精摄入对溃疡愈合过程中颊黏膜bFGF和Cdk2表达的影响。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204512
B L Slomiany, J Piotrowski, A Slomiany

In this study, we investigated the effect of chronic alcohol ingestion on the interplay between the receptor-bound basic fibroblast growth factor (bFGF-R) and the expression of cyclin-dependent kinase (Cdk2) in buccal mucosa during ulcer healing. Chronic ulceration was induced by a topical application of acetic acid to the buccal mucosa of rats maintained for 5 weeks on alcohol-containing or control liquid diet. In both groups, the ulcer healing was accompanied by an increase in buccal mucosal expression of bFGF and Cdk2. In the control group, the ulcer healed within 10 days and maximum induction in bFGF (2.6-fold) and Cdk2 (2.4-fold) occurred by the 2nd day of healing. In contrast, the alcohol diet group showed a marked delay in ulcer healing (14 days), associated with the shift in maximum of bFGF and Cdk2 expression to the 4-6th day, and the values were reduced by 35 to 38%. The findings show that chronic alcohol ingestion exerts detrimental effect on the signaling events initiated by bFGF-receptor activation and propagated by Cdk2 that propels the cell cycle progression essential for rapid mucosal repair.

在这项研究中,我们研究了慢性酒精摄入对口腔溃疡愈合过程中受体结合的碱性成纤维细胞生长因子(bFGF-R)和细胞周期蛋白依赖性激酶(Cdk2)表达之间相互作用的影响。以含酒精或对照液体喂养5周的大鼠,口腔黏膜外用醋酸诱导慢性溃疡。两组溃疡愈合均伴有颊黏膜bFGF和Cdk2表达升高。对照组溃疡在10天内愈合,在愈合第2天出现bFGF(2.6倍)和Cdk2(2.4倍)的最大诱导。相比之下,酒精饮食组溃疡愈合明显延迟(14天),与bFGF和Cdk2表达最大值转移到第4-6天有关,其值降低了35%至38%。研究结果表明,慢性酒精摄入对由bfgf受体激活启动并由Cdk2传播的信号事件产生不利影响,这些信号事件推动了对快速粘膜修复至关重要的细胞周期进程。
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引用次数: 8
Complementation of the growth defect of an rnpA49 mutant of Escherichia coli by overexpression of arginine tRNA(CCG). 通过过表达精氨酸tRNA(CCG)弥补大肠杆菌rnpA49突变体的生长缺陷
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204712
M S Kim, B H Park, S Kim, Y J Lee, J H Chung, Y Lee

We previously found that overexpression of arginine tRNA(CCG) from Brevibacterium albidum complements the rnpA49 mutation, which is responsible for the thermosensitivity of Escherichia coli RNase P function. In this present work, we show that the E. coli homologue tRNA also complements the same mutation, but other tRNAs do not. These results suggest that the rnpA49 mutation causes a major cellular defect in an RNase P reaction to generate the mature arginine tRNA(CCG).

我们之前发现,来自短杆菌的精氨酸tRNA(CCG)的过表达补充了rnpA49突变,该突变负责大肠杆菌RNase P功能的热敏性。在目前的工作中,我们发现大肠杆菌同源tRNA也可以补充相同的突变,但其他tRNA不能。这些结果表明,rnpA49突变导致RNase P反应中产生成熟精氨酸tRNA(CCG)的主要细胞缺陷。
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引用次数: 5
Vitamin E protects the brain against oxidative injury stimulated by excessive aluminum intake. 维生素E保护大脑免受过量摄入铝所引起的氧化损伤。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204732
A A Abd el-Fattah, H M al-Yousef, A M al-Bekairi, H A al-Sawaf

The effect of feeding groups of mice with a diet containing 2000, 4000 and 6000 micrograms aluminum (Al3-/g) for two weeks (subacute) or 2000 and 4000 micrograms Al3+/g for eight weeks (subchronic) as well as the coadministration of vitamin E (alpha-tocopherol) 500 micrograms/g with Al3+, on the status of glutathione (GSH) and lipid peroxides as thiobarbituric acid reactive substances (TBARS) in whole brain tissues were evaluated. Changes in TBARS were further evaluated in vitro following the incubation of brain homogenates of the Al(3+)-fed mice in the presence of 50 microM FeSO4. The results of subacute experiments revealed that the brain levels of GSH were significantly decreased only in the group of mice that received 6000 micrograms Al3+/g diet (P < 0.05) and this effect was partially ameliorated when vitamin E was coadministered with Al3+. TBARS were significantly increased in vitro only in the presence of free iron ions and depended on the concentration of Al3+ in the diet. The effect was opposed by the vitamin E intake. Following subchronic Al3+ intake, the GSH content of the brain was significantly decreased only in the group of mice that received 4000 micrograms Al3+/g diet (P < 0.01), while TBARS were significantly increased in the brain tissues in vivo as well as in the presence of free iron ions in vitro. However, coadministration of vitamin E with Al3+ for eight weeks preserved GSH levels and decreased TBARS in the brain of mice in vivo and in the presence of free iron ions in vitro. It is concluded that the long term administration of vitamin E may prevent Al3(+)-stimulated oxidative injury in the brain.

以2000、4000和6000微克铝(Al3-/g)喂养2周(亚急性)或2000和4000微克铝(Al3 +/g)喂养8周(亚慢性),并与500微克铝(α -生育酚)同时给予全脑组织谷胱甘肽(GSH)和脂质过氧化物作为硫代巴比妥酸反应物质(TBARS)的状态进行了研究。将Al(3+)喂养小鼠的脑匀浆在50微米FeSO4存在下孵育后,在体外进一步评估TBARS的变化。亚急性实验结果显示,仅在6000微克Al3+/g饮食组小鼠脑内谷胱甘肽水平显著降低(P < 0.05),维生素E与Al3+共同给药可部分改善这种影响。体外实验中,TBARS仅在游离铁离子存在的情况下显著增加,且与饲料中Al3+的浓度有关。这种效果与维生素E的摄入量相反。亚慢性Al3+摄入后,只有4000微克Al3+/g组脑组织GSH含量显著降低(P < 0.01),而体内及体外游离铁离子存在时脑组织TBARS均显著升高。然而,在体内和体外存在游离铁离子的情况下,维生素E与Al3+共给药8周,小鼠大脑中GSH水平保持不变,TBARS降低。由此可见,长期服用维生素E可预防Al3(+)刺激的脑氧化损伤。
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引用次数: 31
Inhibition studies on membrane adenosine deaminase from human placenta. 人胎盘膜腺苷脱氨酶的抑制研究。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204622
G Lupidi, F Marmocchi, G Cristalli

The ecto form of adenosine deaminase isolated from human placental membrane was tested towards its sensitivity against adenosine deaminase inhibitors, such as aza and deaza analogues of adenosine and erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA). Ki values of the inhibitors observed were similar to these obtained for the small form of adenosine deaminase purified from human erythrocytes, indicating that the presence of the binding protein on placental adenosine deaminase does not produce alteration in the binding of these inhibitors on the enzyme active site. The inhibition rate of 2'-deoxycoformycin, one of the most potent ADA inhibitors is affected by the presence of the binding protein on human placental adenosine deaminase, that probably modulates the rearrangement of the active site produced by the binding with this tight-binding inhibitor.

从人胎盘膜中分离的腺苷脱氨酶外泌体对腺苷脱氨酶抑制剂(如腺苷和红-9-(2-羟基-3-壬基)腺嘌呤(EHNA)的aza和deaza类似物)的敏感性进行了测试。观察到的抑制剂的Ki值与从人红细胞中纯化的小形式腺苷脱氨酶的Ki值相似,表明胎盘腺苷脱氨酶结合蛋白的存在不会改变这些抑制剂在酶活性位点的结合。人类胎盘腺苷脱氨酶上的结合蛋白的存在影响了2′-脱氧科formycin(最有效的ADA抑制剂之一)的抑制率,这可能调节了与这种紧密结合抑制剂结合时产生的活性位点重排。
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引用次数: 6
The shortening of the N-terminus of myosin essential light chain A1 influences the interaction of heavy meromyosin with actin. 肌凝蛋白必需轻链A1 n端缩短影响重肌凝蛋白与肌动蛋白的相互作用。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204652
N N Efimova, D Stepkowski, H Nieznańska, Y S Borovikov

The effects resulting from the removal of the N-terminus of heavy meromyosin (HMM) A1 light chain by papain digestion are investigated. The fluorometry of TRITC-phalloidin labelled actin in ghost fibers is used as a tool for sensing conformational changes of rigor complex of phosphorylated and dephosphorylated HMM with actin filament. The experiments were performed both under conditions assuring saturation of RLC with magnesium cation (4 mM EGTA) or calcium cation (0.1 mM CaCl2), and in constant presence of 1 mM magnesium chloride. HMM native and with A1 shortened from the N-terminus is used. As it was observed previously rigor complex of actin filament and native HMM shows sensitivity to the kind of cation saturating RLC and to the phosphorylation status of RLC. In particular, the sin2 theta parameter of actin bound rhodamine-phalloidin fluorescence polarization representing roughly the flexibility of actin filament HMM complex changes significantly with the changes of RLC phosphorylation and cation saturation. Removal of the N-terminus of A1 reduces this sensitivity to cation and phosphorylation both in the case of dephosphorylated and phosphorylated HMM. Our results suggest that the N-terminus of A1 plays significant role in the rigor interaction of myosin heads with actin and is involved in modulatory function of RLC in this interaction.

研究了木瓜蛋白酶消化去除重肌球蛋白(HMM) A1轻链n端所产生的影响。鬼纤维中TRITC-phalloidin标记的肌动蛋白荧光测定法被用作检测磷酸化和去磷酸化HMM与肌动蛋白丝的严格复合物构象变化的工具。实验在镁离子(4mm EGTA)或钙离子(0.1 mM CaCl2)饱和RLC的条件下进行,并在1mm氯化镁的恒定存在下进行。HMM原生和A1从n端缩短使用。正如之前观察到的那样,肌动蛋白丝和天然HMM的严格复合物对阳离子饱和RLC的种类和RLC的磷酸化状态表现出敏感性。特别是,大致代表肌动蛋白丝状HMM复合物柔韧性的肌动蛋白结合罗丹明-phalloidin荧光偏振sin2 theta参数随着RLC磷酸化和阳离子饱和度的变化而发生显著变化。在去磷酸化和磷酸化HMM的情况下,去除A1的n端降低了这种对阳离子和磷酸化的敏感性。我们的研究结果表明,A1的n端在肌凝蛋白头与肌动蛋白的严格相互作用中起重要作用,并参与RLC在这种相互作用中的调节功能。
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引用次数: 5
The plasma membrane Fe(3+)-reductase activity of Caco-2 cells is modulated during differentiation. Caco-2细胞的质膜Fe(3+)-还原酶活性在分化过程中受到调节。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204502
C Ekmekcioglu, G Strauss-Blasche, W Marktl

The aim of the present study was to investigate whether the brush border membrane ferric reductase activity of Caco-2 cells is modulated during cell differentiation. The ferric reductase activity was determined in whole cells and isolated microvillous membranes at different stages of cell differentiation by measuring the amount of Fe3+ reduced during the incubation time. Our results indicated that the ferric reductase activity decreased in fastly growing cells and reactivated in postconfluent cells in contrast to the alkaline phosphatase and sucrase activities which were progressively expressed during differentiation as conventional indicators of cell maturity. The lowest ferric reductase activity was found in cells at the log phase of proliferation, while freshly seeded or highly differentiated cells had significantly higher enzyme activities. Cells grown under serum-free conditions had similar ferric iron reduction rates as cells propagated under standard conditions. Reagents or hormones affecting cell metabolism through different pathways had no significant effect on this transplasma membrane redox system.

本研究的目的是探讨Caco-2细胞的刷状缘膜铁还原酶活性是否在细胞分化过程中受到调节。通过测定培养时间内铁还原酶的减少量,测定细胞分化不同阶段全细胞和离体微绒毛膜中铁还原酶的活性。我们的研究结果表明,与碱性磷酸酶和蔗糖酶活性相比,铁还原酶活性在快速生长的细胞中下降,并在融合后的细胞中重新激活,而碱性磷酸酶和蔗糖酶活性在分化过程中逐渐表达,作为细胞成熟的常规指标。在增殖对数期细胞中,铁还原酶活性最低,而新鲜播种或高度分化的细胞中,铁还原酶活性显著较高。在无血清条件下生长的细胞与在标准条件下繁殖的细胞具有相似的铁还原率。通过不同途径影响细胞代谢的试剂或激素对这一跨质膜氧化还原系统无显著影响。
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引用次数: 6
Gene transfer via pollen-tube pathway for anti-fusarium wilt in watermelon. 西瓜抗枯萎病花粉管途径基因转移。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204762
W S Chen, C C Chiu, H Y Liu, T L Lee, J T Cheng, C C Lin, Y J Wu, H Y Chang

In order to obtain transgenic fusarium wilt resistant watermelon plants, squash DNA was introduced into the ovaries of watermelon plants via the pollen-tube pathway. The introduction of foreign genes into ovaries was accomplished using co-transformation with the CaMV35S-GUS as a marker. Transformed watermelon plants contained integrated copies of the GUS activity and the seeds of transformed progeny produced a blue color when stained with 5-bromo-4-chloro-3-indolyl glucuronide, whereas seeds from untransformed control plants did not. Of 200 transformed seedlings, ten were wilt resistant. The presence of the GUS activity in the genome of stable transgenic seedlings was confirmed by Southern blot analysis. Furthermore, the generation of random amplified polymorphic DNA (RAPD) fingerprints using primers with embedded restriction sites showed amplification products unique to these transgenic plants. Primers OPA-1 and OPA-9 gave distinct band patterns of genomic DNA using the polymerase chain reaction.

为了获得抗枯萎病转基因西瓜植株,通过花粉管途径将南瓜DNA导入西瓜植株子房。以CaMV35S-GUS为标记共转化,完成外源基因导入子房。转化后的西瓜植株含有GUS活性的完整拷贝,并且在5-溴-4-氯-3-吲哚基葡萄糖醛酸盐染色时,转化后代的种子产生蓝色,而未转化的对照植株的种子则没有。在200株转化的幼苗中,有10株具有抗枯萎性。经Southern blot分析证实,稳定的转基因幼苗基因组中存在GUS活性。此外,利用嵌入限制性内切位点的引物生成的随机扩增多态性DNA (RAPD)指纹图谱显示了这些转基因植物特有的扩增产物。引物OPA-1和OPA-9通过聚合酶链反应得到了不同的基因组DNA带型。
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引用次数: 38
Characterization of mouse ubiquitin-like SMT3A and SMT3B cDNAs and gene/pseudogenes. 小鼠泛素样SMT3A和SMT3B cdna及基因/假基因的表征。
Pub Date : 1998-12-01 DOI: 10.1080/15216549800204722
A Chen, H Mannen, S S Li

Mouse SMT3A and SMT3B cDNAs encoding ubiquitin-like proteins of 110 and 95 amino acids, respectively, were isolated and sequenced. The sequence of the first 92 amino acids (ending with the conserved Gly-Gly) of mouse SMT3A exhibited two differences at amino acid no. 38 and 76 in comparison with that of human SMT3A. The C-terminal 18 amino acid sequence of mouse SMT3A was completely different from the C-terminal 11 amino acid sequence of human SMT3A. Mouse and human SMT3B were identical for a sequence of 95 amino acids. Mouse SMT3A genomic DNAs were amplified by polymerase-chain-reaction and sequenced. The nucleotide sequence of a PCR-amplified SMT3A genomic DNA fragment was found to be identical to that of SMT3A cDNA, indicating the absence of intron(s) in its protein coding region. Another genomic DNA fragment of 1,531 nucleotides, containing 7% differences from that of cDNA, is unable to encode a functional protein, and thus, it is a SMT3A processed pseudogene. Three mouse SMT3B processed pseudogenes were cloned and sequenced. The genuine mouse SMT3B gene has not yet been isolated. Mouse SMT3A transcript of 1.8 kb was predominantly expressed in most tissues, while SMT3B transcript of 1.0 kb was abundantly present in all tissues analyzed. A family of ubiquitin-like proteins was recently discovered. One distinguishing feature of ubiquitin and ubiquitin-like proteins is the capacity to conjugate with other proteins post-translationally. The ubiquitin-like proteins are cleaved endoproteolytically after a diglycine sequence, corresponding to the C-terminal Gly75-Gly76 of ubiquitin. The cleavage activates the molecule for conjugation. The yeast SMT3 gene was originally identified as a suppressor of mutations in MIF2 gene, which encodes an essential protein binding to the A+T-rich CDEII region of centromere DNA (1). Studies using temperature-sensitive mutants showed that the loss of yeast Mif2 protein function results in chromosome missegregation, mitotic delay, and aberrant microtubule morphologies (2). The yeast Mif2 protein shares at least two regions of similarity with mammalian centromere protein CENP-C, an integral component of active kinetochores (3, 4). Human SMT3A cDNA was identified from the genome sequencing project of chromosome 21 (5). We have cloned human SMT3B (formerly designated as HSMT3) cDNA (6). Human SMT3C protein was independently isolated by several groups and denoted as SUMO-1 (7), GMP1 (8), PICI (9), UBL1 (10), sentrin (11). SUMO-1/GMP1 was found to be covalently linked to the Ran GTPase-activating protein RanGAP1, and attachment of SUMO-1 targets the otherwise cytosolic RanGAP1 to the nuclear pore complex. The modified form of RanGAP1 also appeared to associate with the mitotic spindle apparatus during mitosis (7, 8). PIC1 was shown to interact with the PML component of nuclear multiprotein complex that is disrupted in acute promyelocytic leukemia (9). UBL1 was found to associate with human RAD51/RAD52 proteins involved

小鼠SMT3A和SMT3B cdna分别编码110和95个氨基酸的泛素样蛋白,并进行了分离和测序。小鼠SMT3A的前92个氨基酸序列(以保守的Gly-Gly结尾)在第2号氨基酸上存在两个差异。与人类的SMT3A相比,分别为38和76。小鼠SMT3A的c -末端18氨基酸序列与人类SMT3A的c -末端11氨基酸序列完全不同。小鼠和人类的SMT3B在95个氨基酸序列上是相同的。采用聚合酶链反应扩增小鼠SMT3A基因组dna并测序。pcr扩增的SMT3A基因组DNA片段的核苷酸序列与SMT3A cDNA的核苷酸序列相同,表明其蛋白质编码区不含内含子。另一个1531个核苷酸的基因组DNA片段,与cDNA有7%的差异,不能编码功能蛋白,因此,它是一个SMT3A加工的假基因。克隆并测序了3个SMT3B加工的小鼠假基因。真正的小鼠SMT3B基因尚未被分离出来。小鼠1.8 kb的SMT3A转录本在大多数组织中主要表达,而1.0 kb的SMT3B转录本在所有分析的组织中都大量存在。最近发现了一个泛素样蛋白家族。泛素和泛素样蛋白的一个显著特征是翻译后与其他蛋白结合的能力。泛素样蛋白在二甘氨酸序列后被蛋白内水解裂解,对应于泛素的c端Gly75-Gly76。裂解激活分子偶联。酵母SMT3基因最初被鉴定为MIF2基因突变的抑制因子,MIF2基因编码一种与着丝粒DNA富含a + t的CDEII区域结合的必需蛋白(1)。使用温度敏感突变体的研究表明,酵母MIF2蛋白功能的丧失导致染色体错分离、有丝分裂延迟和微管形态异常(2)。酵母MIF2蛋白与哺乳动物着丝粒蛋白CENP-C至少有两个相似区域。人类SMT3A cDNA是从21号染色体的基因组测序项目中鉴定出来的(5)。我们克隆了人类SMT3B(以前称为HSMT3) cDNA(6)。人类SMT3C蛋白被几个小组独立分离出来,分别为SUMO-1(7)、GMP1(8)、PICI(9)、UBL1(10)、sentrin(11)。SUMO-1/GMP1被发现与Ran gtpase激活蛋白RanGAP1共价连接,并且SUMO-1的附着将细胞质RanGAP1靶向到核孔复合物上。在有丝分裂过程中,RanGAP1的修饰形式似乎也与有丝分裂纺锤体有关(7,8)。PIC1被证明与急性早髓细胞白血病中被破坏的核多蛋白复合物的PML组分相互作用(9)。UBL1被发现与参与DNA重组和DNA双链断裂修复的人类RAD51/RAD52蛋白有关(10)。研究表明,Sentrin与Fas/APO-1或TNF受体1死亡结构域相互作用,Sentrin的过表达对抗Fas/APO-1和TNF诱导的细胞死亡都有保护作用(11)。在这里,我们报告了小鼠SMT3A和SMT3B cdna,基因/假基因和mRNA表达的表征。
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引用次数: 42
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Biochemistry and molecular biology international
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