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The betaII isotype of tubulin is present in the cell nuclei of a variety of cancers. 微管蛋白的β i同型存在于多种癌症的细胞核中。
Pub Date : 2004-02-01 DOI: 10.1002/cm.10157
I-Tien Yeh, Richard F Ludueña

Tubulin, the subunit protein of microtubules, has generally been thought to be exclusively a cytoplasmic protein in higher eukaryotes. We have previously shown that cultured rat kidney mesangial cells contain the betaII isotype of tubulin in their nuclei in the form of an alphabetaII dimer [Walss et al., 1999: Cell Motil. Cytoskeleton 42:274-284, 1999]. More recently, we examined a variety of cancerous and non-cancerous cell lines and found betaII in the nuclei of all of the former and only a few of the latter (Walss-Bass et al., 2002: Cell Tissue Res. 308:215-223]. In order to determine if betaII-tubulin occurs in the nuclei of actual cancers as well as in cancer cell lines, we used the immunoperoxidase method to look for nuclear betaII in a variety of tumors excised from 201 patients. We found that 75% of these tumors contain betaII in their nuclei. Distribution of nuclear betaII was highly dependent on the type of cancer, with 100% of the colon and prostate cancers, but only 19% of the skin tumors, having nuclear betaII. Nuclear betaII was particularly marked in tumors of epithelial origin, of which 83% showed nuclear betaII, in contrast to 54% in tumors of non-epithelial origin. In many cases, betaII staining occurred very strongly in the nuclei and not in the cytoplasm; in other cases, betaII was present in both. In many cases, particularly metastases, otherwise normal cells adjacent to the tumor also showed nuclear betaII, suggesting that cancer cells may influence nearby cells to synthesize betaII and localize it to their nuclei. Our results have implications for the diagnosis, biology, and chemotherapy of cancer.

微管蛋白是微管的亚基蛋白,通常被认为是高等真核生物的细胞质蛋白。我们之前已经证明,培养的大鼠肾系膜细胞在其细胞核中含有β i同型微管蛋白,其形式为α i二聚体[Walss等人,1999:Cell Motil]。中国生物医学工程学报,1999]。最近,我们研究了多种癌性和非癌性细胞系,发现β i存在于所有癌性和非癌性细胞系的细胞核中,而只有少数癌性细胞系的细胞核中存在β i (walsh - bass et al., 2002: cell Tissue Res. 308:215-223)。为了确定betaII-微管蛋白是否存在于实际癌症的细胞核以及癌细胞系中,我们使用免疫过氧化物酶方法在201例患者切除的多种肿瘤中寻找核betaII。我们发现75%的肿瘤细胞核中含有β i。核β i的分布高度依赖于癌症的类型,100%的结肠癌和前列腺癌,但只有19%的皮肤肿瘤含有核β i。核betaII在上皮来源的肿瘤中特别明显,其中83%的肿瘤显示核betaII,而在非上皮来源的肿瘤中这一比例为54%。在许多情况下,β i染色强烈地发生在细胞核而不是细胞质中;在其他情况下,betaII在两种情况下都存在。在许多情况下,特别是转移性肿瘤,肿瘤周围正常的细胞也显示出核betaII,这表明癌细胞可能影响附近的细胞合成betaII并将其定位到细胞核中。我们的研究结果对癌症的诊断、生物学和化疗都有意义。
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引用次数: 47
Aneuploidy, the somatic mutation that makes cancer a species of its own. 非整倍体,使癌症成为一个独立物种的体细胞突变。
Pub Date : 2000-10-01 DOI: 10.1002/1097-0169(200010)47:2<81::AID-CM1>3.0.CO;2-#
P Duesberg, D Rasnick

The many complex phenotypes of cancer have all been attributed to "somatic mutation." These phenotypes include anaplasia, autonomous growth, metastasis, abnormal cell morphology, DNA indices ranging from 0.5 to over 2, clonal origin but unstable and non-clonal karyotypes and phenotypes, abnormal centrosome numbers, immortality in vitro and in transplantation, spontaneous progression of malignancy, as well as the exceedingly slow kinetics from carcinogen to carcinogenesis of many months to decades. However, it has yet to be determined whether this mutation is aneuploidy, an abnormal number of chromosomes, or gene mutation. A century ago, Boveri proposed cancer is caused by aneuploidy, because it correlates with cancer and because it generates "pathological" phenotypes in sea urchins. But half a century later, when cancers were found to be non-clonal for aneuploidy, but clonal for somatic gene mutations, this hypothesis was abandoned. As a result aneuploidy is now generally viewed as a consequence, and mutated genes as a cause of cancer although, (1) many carcinogens do not mutate genes, (2) there is no functional proof that mutant genes cause cancer, and (3) mutation is fast but carcinogenesis is exceedingly slow. Intrigued by the enormous mutagenic potential of aneuploidy, we undertook biochemical and biological analyses of aneuploidy and gene mutation, which show that aneuploidy is probably the only mutation that can explain all aspects of carcinogenesis. On this basis we can now offer a coherent two-stage mechanism of carcinogenesis. In stage one, carcinogens cause aneuploidy, either by fragmenting chromosomes or by damaging the spindle apparatus. In stage two, ever new and eventually tumorigenic karyotypes evolve autocatalytically because aneuploidy destabilizes the karyotype, ie. causes genetic instability. Thus, cancer cells derive their unique and complex phenotypes from random chromosome number mutation, a process that is similar to regrouping assembly lines of a car factory and is analogous to speciation. The slow kinetics of carcinogenesis reflects the low probability of generating by random chromosome reassortments a karyotype that surpasses the viability of a normal cell, similar again to natural speciation. There is correlative and functional proof of principle: (1) solid cancers are aneuploid; (2) genotoxic and non-genotoxic carcinogens cause aneuploidy; (3) the biochemical phenotypes of cells are severely altered by aneuploidy affecting the dosage of thousands of genes, but are virtually un-altered by mutations of known hypothetical oncogenes and tumor suppressor genes; (4) aneuploidy immortalizes cells; (5) non-cancerous aneuploidy generates abnormal phenotypes in all species tested, e.g., Down syndrome; (6) the degrees of aneuploidies are proportional to the degrees of abnormalities in non-cancerous and cancerous cells; (7) polyploidy also varies biological phenotypes; (8) variation of the numbers of chromosomes is the basis

许多复杂的癌症表型都归因于“体细胞突变”。这些表型包括发育不全、自主生长、转移、细胞形态异常、DNA指数从0.5到2以上、克隆起源但不稳定和非克隆核型和表型、中心体数量异常、在体外和移植中不朽、恶性肿瘤的自发进展以及从致癌物到癌变的极慢动力学(数月至数十年)。然而,这种突变是非整倍体、染色体数目异常还是基因突变还有待确定。一个世纪前,Boveri提出癌症是由非整倍体引起的,因为它与癌症相关,并且在海胆中产生“病理”表型。但半个世纪后,当癌症被发现是非整倍体的非克隆性,而体细胞基因突变的克隆性时,这个假设被抛弃了。因此,非整倍体现在普遍被认为是一种结果,而突变的基因是导致癌症的原因,尽管:(1)许多致癌物不会使基因突变,(2)没有功能上的证据表明突变的基因会导致癌症,(3)突变是快速的,但致癌是非常缓慢的。被非整倍体巨大的致突变潜力所吸引,我们对非整倍体和基因突变进行了生化和生物学分析,结果表明非整倍体可能是唯一可以解释癌变所有方面的突变。在此基础上,我们现在可以提供一个连贯的两阶段癌变机制。在第一阶段,致癌物通过分裂染色体或破坏纺锤体引起非整倍体。在第二阶段,由于非整倍性破坏了核型的稳定性,新的和最终致瘤性的核型会自动催化进化。导致基因不稳定。因此,癌细胞从随机染色体数目突变中获得独特而复杂的表型,这一过程类似于汽车厂装配线的重组,类似于物种形成。癌变的缓慢动力学反映了通过随机染色体重组产生超过正常细胞生存能力的核型的低概率,再次类似于自然物种形成。有相关的和功能的原理证明:(1)实体癌是非整倍体;(2)基因毒性和非基因毒性致癌物引起非整倍体;(3)细胞的生化表型受到影响数千个基因剂量的非整倍体的严重改变,但实际上不受已知假设的致癌基因和肿瘤抑制基因突变的影响;(4)非整倍性使细胞不朽;(5)非癌性非整倍体在所有被测物种中产生异常表型,例如唐氏综合征;(6)非整倍体的程度与非癌细胞和癌变细胞的异常程度成正比;(7)多倍体也改变生物学表型;(8)染色体数目的变化是物种形成的基础。因此,非整倍性属于物种形成的定义,癌症是一个自己的物种。非整倍体假说为癌症预防和治疗提供了新的前景。
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引用次数: 240
Vigorous beating of Chlamydomonas axonemes lacking central pair/radial spoke structures in the presence of salts and organic compounds. 缺乏中心对/辐射状辐状结构的衣藻轴突在盐和有机化合物存在下剧烈跳动。
Pub Date : 2000-07-01 DOI: 10.1002/1097-0169(200007)46:3<190::AID-CM4>3.0.CO;2-#
T Yagi, R Kamiya

Flagella of Chlamydomonas mutants lacking the central pair of microtubules or radial spokes do not beat; however, axonemes isolated from these mutants were found to display vigorous bending movements in the presence of ATP and various salts, sugars, alcohols, and other organic compounds. For example, about 15% of the total axonemes isolated from pf18, a mutant lacking the central pair, displayed beating in the presence of 10 mM MgSO(4) and 0.2 mM ATP at about 22 Hz, while none beat with the same concentration of ATP and < or = 5 mM or > or = 25 mM MgSO(4). The beat frequency and waveform of beating pf18 axonemes were similar to those of wild type axonemes beating under the same conditions. Similarly, 10-50% of the axonemes beat in the presence of 0.5 M sucrose, 2.0 M glycerol, or 1.7 M[10% (v/v)] ethanol. The appearance of motility did not correlate with the change in axonemal ATPase; however, these substances at those concentrations commonly increased the amplitude of nanometer-scale oscillation (hyper-oscillation) in pf18 axonemes, as well as the extent of ATP-induced sliding disintegration of protease-treated axonemes. Axonemes of double mutants lacking both the central pair and various subspecies of inner-arm dynein also beat at increased MgSO(4) concentrations, but axonemes lacking outer-arm dynein in addition to the central pair did not beat. These and other observations suggest that small molecules perturb the regulation of microtubule sliding through some change in water activity or osmotic stress. Axonemes must have an intrinsic ability to beat without the central pair/radial spokes under a variety of non-physiological solution conditions, as long as the outer dynein arms are present. Apparently, the major function of the central pair/radial spoke structures is to restore this activity under physiological conditions.

突变衣藻的鞭毛缺乏中央对微管或放射状辐条不跳动;然而,从这些突变体中分离出来的轴突体在ATP和各种盐、糖、醇和其他有机化合物的存在下显示出剧烈的弯曲运动。例如,从缺乏中心对的突变体pf18中分离出的总轴突体中,约有15%在10mm MgSO(4)和0.2 mM ATP(约22 Hz)存在下显示跳动,而在相同浓度的ATP和<或= 5 mM或>或= 25 mM MgSO(4)下没有跳动。pf18轴突的跳动频率和波形与野生型轴突在相同条件下的跳动频率和波形相似。同样,10-50%的轴突蛋白在0.5 M蔗糖、2.0 M甘油或1.7 M[10% (v/v)]乙醇的存在下也能发酵。运动的出现与轴突atp酶的变化无关;然而,这些物质在这些浓度下通常会增加pf18轴突的纳米级振荡幅度(超振荡),以及atp诱导的蛋白酶处理轴突滑动解体的程度。当MgSO(4)浓度增加时,缺乏中心对和内臂动力蛋白各亚种的双突变体轴突组也会跳动,但除了中心对外缺乏外臂动力蛋白的轴突组不会跳动。这些和其他观察结果表明,小分子通过水活性或渗透应力的一些变化扰乱了微管滑动的调节。轴突体必须具有内在的能力,在各种非生理溶液条件下,只要外部动力蛋白臂存在,轴突体就可以在没有中心副/径向辐条的情况下跳动。显然,中央对/径向辐条结构的主要功能是在生理条件下恢复这种活动。
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引用次数: 53
Forced expression of a dominant-negative chimeric tropomyosin causes abnormal motile behavior during cell division. 强迫表达的显性负嵌合原肌球蛋白导致异常运动行为在细胞分裂。
Pub Date : 2000-02-01 DOI: 10.1002/(SICI)1097-0169(200002)45:2<121::AID-CM4>3.0.CO;2-#
K Wong, D Wessels, S L Krob, A R Matveia, J L Lin, D R Soll, J J Lin

Forced expression of the chimeric human fibroblast tropomyosin 5/3 (hTM5/3) in CHO cell was previously shown to affect cytokinesis [Warren et al., 1995: J. Cell Biol. 129:697-708]. To further investigate the phenotypic consequences of misexpression, we have compared mitotic spindle organization and dynamic 2D and 3D shape changes during mitosis in normal cells and in a hTM5/3 misexpressing (mutant) cell line. Immunofluorescence microscopy of wild type and mutant cells stained with monoclonal anti-tubulin antibody revealed that the overall structures of mitotic spindles were not significantly different. However, the axis of the mitotic spindle in mutant cells was more frequently misaligned with the long axis of the cell than that of wild type cells. To assess behavioral differences during mitosis, wild type and mutant cells were reconstructed in 2D and 3D and motion analyzed with the computer-assisted 2D and 3D Dynamic Image Analysis Systems (2D-DIAS, 3D-DIAS). Mutant cells abnormally formed large numbers of blebs during the later stages of mitosis and took longer to proceed from the start of anaphase to the start of cytokinesis. Furthermore, each mutant cell undergoing mitosis exhibited greater shape complexity than wild type cells, and in every case lifted one of the two evolving daughter cells off the substratum and abnormally twisted. These results demonstrate that misexpression of hTM5/3 in CHO cells leads to morphological instability during mitosis. Misexpression of hTM5/3 interferes with normal tropomyosin function, suggesting in turn that tropomyosin plays a role through its interaction with actin microfilaments in the regulation of the contractile ring, in the localized suppression of blebbing, in the maintenance of polarity and spatial symmetry during cytokinesis, and in cell spreading after cytokinesis is complete.

人类成纤维细胞原肌球蛋白5/3 (hTM5/3)在CHO细胞中的表达对细胞动力学的影响[j].中国生物医学工程学报,1995,29(1):697- 698。为了进一步研究错误表达的表型后果,我们比较了正常细胞和hTM5/3错误表达(突变)细胞系有丝分裂过程中纺锤体组织和动态二维和三维形状的变化。用单克隆抗微管蛋白抗体染色对野生型和突变型细胞进行免疫荧光显微镜观察,发现有丝分裂纺锤体的整体结构无明显差异。然而,与野生型细胞相比,突变型细胞的有丝分裂纺锤体轴更频繁地与细胞的长轴错位。为了评估有丝分裂过程中的行为差异,在2D和3D中重建野生型和突变型细胞,并使用计算机辅助的2D和3D动态图像分析系统(2D- dias, 3D- dias)分析运动。突变细胞在有丝分裂后期异常形成大量泡,从后期开始到胞质分裂开始需要更长的时间。此外,每个进行有丝分裂的突变细胞都比野生型细胞表现出更大的形状复杂性,并且在每种情况下都将两个进化的子细胞中的一个从基质中剥离出来并异常扭曲。这些结果表明,hTM5/3在CHO细胞中的错误表达导致有丝分裂过程中的形态不稳定。htm4 /3的错表达干扰了原肌球蛋白的正常功能,提示原肌球蛋白通过与肌动蛋白微丝的相互作用,参与调节收缩环,局部抑制泡,维持细胞分裂过程中的极性和空间对称性,以及细胞分裂完成后的细胞扩散。
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引用次数: 20
Movement of turritella spermatozoa: direction of propagation and chirality of flagellar bends. 菱形精子的运动:繁殖方向和鞭毛弯曲的手性。
Pub Date : 1999-10-01 DOI: 10.1002/(SICI)1097-0169(199910)44:2<85::AID-CM1>3.0.CO;2-#
S Ishijima, S A Ishijima, B A Afzelius

The marine snail, Turritella communis, produces two types of spermatozoa, named apyrene and eupyrene. Eupyrene spermatozoa are usually paired, but unpaired ones are involved in fertilization. Movements of these spermatozoa were analyzed using a video camera with a high-speed shutter. The eupyrene spermatozoa usually swim with the head foremost but are able to swim flagellum foremost. A reversal of the direction of their swimming was found to be the result of a change in the direction of flagellar bend propagation, which changed with calcium concentration. Reversal of the direction of bend propagation was accompanied by a reversal of direction of the rotational movement of the spermatozoa around their long axis, suggesting that the bending waves keep the sense of their three-dimensional form. The swimming speed of apyrene spermatozoa in natural seawater was about one-eighth of that of the eupyrene ones and remained almost constant in highly viscous medium. The swimming speed of conjugated eupyrene spermatozoa was the same as that of unpaired spermatozoa over a wide viscosity range (<3,000 cP). No advantage of swimming by two spermatozoa could be detected in Turritella spermatozoa.

海蜗牛Turritella communis能产生两种精子,分别是apyrene和eupyrene。真丝精子通常是成对的,但未成对的精子参与受精。使用高速快门的摄像机分析这些精子的运动。真核精子通常头在前游动,但鞭毛在前游动。研究发现,它们游动方向的逆转是鞭毛弯曲繁殖方向发生变化的结果,而鞭毛弯曲繁殖方向随着钙浓度的变化而变化。弯曲传播方向的逆转伴随着精子绕其长轴旋转运动方向的逆转,这表明弯曲波保持了其三维形式的感觉。无炔精子在自然海水中的游动速度约为真炔精子的八分之一,在高粘性介质中几乎保持不变。在较宽的黏度范围内,共轭真核精子的游动速度与未配对精子的游动速度相同(
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引用次数: 21
Microtubule severing. 微管切断。
Pub Date : 1999-01-01 DOI: 10.1002/(sici)1097-0169(1999)43:1<1::aid-cm1>3.0.co;2-
L. Quarmby, T. A. Lohret
The regulation of microtubule stability by severing of the polymer along its length is a newly appreciated and potentially important mechanism for controlling microtubule function. Microtubule severing occurs in living cells, but direct observation of this event is infrequent. The paucity of direct observations leave open to question the significance of regulated microtubule severing in the control of microtubule organization. Nevertheless, several lines of evidence suggest that microtubule severing is an important cellular activity. First, the ATP-dependent microtubule-severing activity of katanin is well documented. Katanin is found in most cell types and is enriched at MTOCs. Although it is possible that katanin does not sever microtubules in vivo, this seems unlikely. Second, a physiological event, deflagellation, has been shown to depend on microtubule severing. The deflagellation system of Chlamydomonas has provided a genetic approach to the problem of microtubule severing. The FA genes are essential for the regulated severing of axonemal microtubules during deflagellation, but whether these genes define new severing proteins or whether they are important for katanin activity remains to be determined. Microtubule severing is a relatively new area of investigation and there are still many more questions than answers. It is anticipated that the recent cloning of katanin and the introduction of a genetic model system will soon lead to significant breakthroughs in this problem.
通过切断聚合物的长度来调节微管的稳定性是一种新的、潜在的重要的控制微管功能的机制。微管切断发生在活细胞中,但对这一事件的直接观察很少。直接观察的缺乏使微管切断在控制微管组织中的重要性受到质疑。然而,一些证据表明,微管切断是一个重要的细胞活动。首先,katanin的atp依赖性微管切断活性得到了充分的证明。卡他蛋白存在于大多数细胞类型中,在MTOCs富集。虽然卡他蛋白在体内可能不会切断微管,但这似乎不太可能。其次,一个生理事件,爆燃,已被证明依赖于微管切断。衣藻的爆裂系统为解决微管断裂问题提供了一种遗传学途径。FA基因对纤裂过程中轴突微管的调控切断至关重要,但这些基因是否定义新的切断蛋白或它们是否对katanin活性很重要仍有待确定。微管切断是一个相对较新的研究领域,仍然有很多问题比答案。可以预期,最近的克隆katanin和遗传模型系统的引入将很快导致这一问题的重大突破。
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引用次数: 28
Microtubule severing. 微管切断。
Pub Date : 1999-01-01 DOI: 10.1002/(SICI)1097-0169(1999)43:1<1::AID-CM1>3.0.CO;2-#
L M Quarmby, T A Lohret

The regulation of microtubule stability by severing of the polymer along its length is a newly appreciated and potentially important mechanism for controlling microtubule function. Microtubule severing occurs in living cells, but direct observation of this event is infrequent. The paucity of direct observations leave open to question the significance of regulated microtubule severing in the control of microtubule organization. Nevertheless, several lines of evidence suggest that microtubule severing is an important cellular activity. First, the ATP-dependent microtubule-severing activity of katanin is well documented. Katanin is found in most cell types and is enriched at MTOCs. Although it is possible that katanin does not sever microtubules in vivo, this seems unlikely. Second, a physiological event, deflagellation, has been shown to depend on microtubule severing. The deflagellation system of Chlamydomonas has provided a genetic approach to the problem of microtubule severing. The FA genes are essential for the regulated severing of axonemal microtubules during deflagellation, but whether these genes define new severing proteins or whether they are important for katanin activity remains to be determined. Microtubule severing is a relatively new area of investigation and there are still many more questions than answers. It is anticipated that the recent cloning of katanin and the introduction of a genetic model system will soon lead to significant breakthroughs in this problem.

通过切断聚合物的长度来调节微管的稳定性是一种新的、潜在的重要的控制微管功能的机制。微管切断发生在活细胞中,但对这一事件的直接观察很少。直接观察的缺乏使微管切断在控制微管组织中的重要性受到质疑。然而,一些证据表明,微管切断是一个重要的细胞活动。首先,katanin的atp依赖性微管切断活性得到了充分的证明。卡他蛋白存在于大多数细胞类型中,在MTOCs富集。虽然卡他蛋白在体内可能不会切断微管,但这似乎不太可能。其次,一个生理事件,爆燃,已被证明依赖于微管切断。衣藻的爆裂系统为解决微管断裂问题提供了一种遗传学途径。FA基因对纤裂过程中轴突微管的调控切断至关重要,但这些基因是否定义新的切断蛋白或它们是否对katanin活性很重要仍有待确定。微管切断是一个相对较新的研究领域,仍然有很多问题比答案。可以预期,最近的克隆katanin和遗传模型系统的引入将很快导致这一问题的重大突破。
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引用次数: 0
Fertilization and pronuclear migration in the ctenophore, Beroe ovata. Video supplement. 栉水母的受精和原核迁移。视频的补充。
Pub Date : 1998-01-01
C Rouvière, E Houliston, D Carré, P Chang, C Sardet
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引用次数: 0
The ankyrin-binding domain of CD44s is involved in regulating hyaluronic acid-mediated functions and prostate tumor cell transformation. CD44s的锚蛋白结合域参与调节透明质酸介导的功能和前列腺肿瘤细胞转化。
Pub Date : 1998-01-01 DOI: 10.1002/(SICI)1097-0169(1998)39:3<209::AID-CM4>3.0.CO;2
D. Zhu, L. Bourguignon
CD44 isoforms, such as CD44s (the standard form), contain at least one ankyrin-binding site within the 70-amino acid (aa) cytoplasmic domain and several hyaluronic acid (HA)-binding sites within the extracellular domain. To study the role of CD44s-ankyrin interaction in regulating human prostate tumor cells, we have constructed several CD44s cytoplasmic deletion mutants that lack the ankyrin-binding site(s). These truncated cDNAs were stably transfected into CD44-negative human prostate tumor cells (LNCaP). Our results indicate that a critical region of 15-amino acids (aa) between aa 304 and aa 318 of CD44s is required for ankyrin binding. Biochemical analyses, using competition binding assays with a synthetic peptide containing the 15 aa between aa 304 and aa 318 (NSGNGAVEDRKPSGL), further support the conclusion that this region contains the ankyrin-binding domain of CD44s. Deletion of this 15-aa ankyrin-binding sequence from CD44s results in a drastic reduction of HA-mediated binding/cell adhesion, Src p60 kinase(s) interaction and anchorage-independent growth in soft agar. These findings suggest that the binding of cytoskeletal proteins, such as ankyrin, to the cytoplasmic domain of CD44s plays a pivotal role in regulating HA-mediated functions as well as Src kinase activity and prostate tumor cell transformation.
CD44同工异构体,如CD44(标准形式),在70个氨基酸(aa)的细胞质区域内至少包含一个锚蛋白结合位点,在细胞外区域内包含几个透明质酸(HA)结合位点。为了研究cd44 -锚蛋白相互作用在调节人前列腺肿瘤细胞中的作用,我们构建了几个缺乏锚蛋白结合位点的cd44细胞质缺失突变体。这些截断的cdna被稳定地转染到cd44阴性的人前列腺肿瘤细胞(LNCaP)中。我们的研究结果表明,CD44s的aa 304和aa 318之间的一个15个氨基酸的关键区域是锚蛋白结合所必需的。生化分析进一步证实,该区域含有CD44s的锚蛋白结合结构域,并与位于aa 304和aa 318之间的合成肽(NSGNGAVEDRKPSGL)竞争结合。从CD44s中删除这个15-aa锚定蛋白结合序列会导致ha介导的结合/细胞粘附、Src p60激酶相互作用和软琼脂中锚定非依赖性生长的急剧减少。这些发现表明,细胞骨架蛋白(如锚蛋白)与CD44s细胞质结构域的结合在调节ha介导的功能、Src激酶活性和前列腺肿瘤细胞转化中起着关键作用。
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引用次数: 46
Actin-based vesicle dynamics and exocytosis during wound wall formation. Video supplement. 伤口壁形成过程中肌动蛋白基囊泡动力学和胞吐作用。视频的补充。
Pub Date : 1998-01-01
I Foissner, I K Lichtscheidl, G O Wasteneys
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引用次数: 0
期刊
Cell motility and the cytoskeleton
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