Plant immunity requires conformational changes [corrected] of NPR1 via S-nitrosylation and thioredoxins

Changes in redox status have been observed during immune responses in different organisms, but the associated signaling mechanisms are poorly understood. In plants, these redox changes regulate the conformation of NPR1, a master regulator of salicylic acid (SA)-mediated defense genes. NPR1 is sequestered in the cytoplasm as an oligomer through intermolecular disulfide bonds. We report that S-nitrosylation of NPR1 by S-nitrosoglutathione (GSNO) at cysteine-156 facilitates its oligomerization, which maintains protein homeostasis upon SA induction. Conversely, the SA-induced NPR1 oligomer-to-monomer reaction is catalyzed by thioredoxins (TRXs). Mutations in both NPR1 cysteine-156 and TRX compromised NPR1-mediated disease resistance. Thus, the regulation of NPR1 is through the opposing action of GSNO and TRX. These findings suggest a link between pathogen-triggered redox changes and gene regulation in plant immunity.     

Induction of the c-fos oncogene by thyrotropic hormone in rat thyroid cells in culture

Rat thyroid cells in culture, rendered quiescent by hormone deprivation, can be stimulated to undergo DNA synthesis in the absence of serum by the addition of purified thyrotropin. The primary effect in response to thyrotropin action in thyroid cells is the induction of the c-fos oncogene, followed by c-myc expression. This suggests that thyrotropin acts as a competence growth factor.     

The human c-ras1H oncogene: a mutation in normal and neoplastic tissue from the same patient

The c-ras1H oncogene can be distinguished from its normal cellular counterpart by the loss of a restriction endonuclease site. This sequence alteration is the basis of a rapid screening method for the presence of this oncogene. DNA's from 34 individuals were screened by this method, and all were homozygous for the normal allele. In contrast, DNA from a patient's bladder tumor, as well as DNA from his normal bladder and leukocytes, were heterozygous at that restriction endonuclease site. Further restriction enzyme mapping pinpointed the change in the mutant allele as being one of two nucleotides, either of which would change the 12th amino acid (glycine) in the normal c-ras1H gene product. Point mutations in the codon for this amino acid have previously been described in a bladder tumor cell line and in the viral oncogene v-rasH. These results indicate that the patient carried a c-ras1H oncogene in his germ line, raising the possibility that the c-ras1H oncogene confers a predisposition to neoplasia.     

Translocation and rearrangements of the c-myc oncogene locus in human undifferentiated B-cell lymphomas

The locus for the cellular myc (c-myc) oncogene in humans is located on the region of chromosome 8 that is translocated to chromosome 14 in cells from most undifferentiated B-cell lymphomas. It is shown in this study that the c-myc locus is rearranged in 5 out of 15 cell lines from patients with undifferentiated B-cell lymphomas, and that the rearrangement involves a region at the 5' side of an apparently intact c-myc gene. In at least three patients, this rearranged region appears to contain immunoglobulin heavy chain mu sequences that are located on chromosome 14. The data indicate that this region contains the crossover point between chromosomes 8 and 14. The break point can occur at different positions on both chromosomes among individual cell lines.     

Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient

A single genetic alteration, a guanine-to-cytosine transversion, is responsible for the acquisition of malignant properties by K-ras genes of two human tumor cell lines established from carcinomas of the bladder (A1698) and lung (A2182). As a consequence, arginine instead of the normal glycine is incorporated into the K-ras-coded p21 proteins at amino acid position 12. This mutation creates a restriction enzyme polymorphism that can be used to screen human cells for transforming K-ras genes. This approach was used to identify the mutational event responsible for the malignant activation of a K-ras oncogene in a squamous cell lung carcinoma of a 66-year-old man; this point mutation was not present in either the normal bronchial or parenchymal tissue or in the blood lymphocytes. Hence, malignant activation of a ras oncogene appears to be specifically associated with the development of a human neoplasm.     

人表皮生长因子融合蛋白在干酪乳杆菌中的表达

以干酪乳杆菌作为传递载体,构建表达人表皮生长因子的重组干酪乳杆菌,探讨原位表达特定蛋白的可行性。采用SOE PCR合成人表皮生长因子序列,克隆到干酪乳杆菌表达载体pELWH,构建pELWHhEGF重组质粒,将该质粒电转化干酪乳杆菌宿主,采用Western blot及间接免疫荧光检测目的蛋白的表达,并通过细胞增殖实验验证目的蛋白的生物学活性。结果表明:在重组菌的细胞表面及培养液上清中均检测到SlpA-hEGF融合蛋白,分子质量约55ku;细胞增殖实验显示SlpA-hEGF融合蛋白及干酪乳杆菌上清均能显著促进NIH/3T3细胞的增殖。     

Mutation affecting the 12th amino acid of the c-Ha-ras oncogene product occurs infrequently in human cancer

A point mutation alters the 12th amino acid of the c-Ha-ras oncogene product p21 in a human bladder cancer cell line. This is, at present, the only mutation known to result in a human transforming gene. This mutation may therefore represent a possible target for mutagenesis leading to carcinogenesis in humans. By means of restriction enzyme analysis, 29 human cancers, including 20 primary tumor tissues, derived from organs commonly exposed to environmental carcinogens, were tested for the presence of this mutation. None of ten primary bladder carcinomas exhibited the mutation; nor did nine colon carcinomas or ten carcinomas of the lung. Thus the point mutation affecting the 12th amino acid of the c-Ha-ras gene product, while a valuable model for carcinogenesis, does not appear to play a role in the development of most human epithelial cancers of the bladder, colon, or lung.     

Gonadotropin-releasing hormone binding sites in human breast carcinoma

Gonadotropin-releasing hormone analogs can cause regression of hormone-dependent breast carcinomas. These effects are thought to be mediated through the inhibition of gonadotropic and steroid hormones. These analogs may also act directly on the tumor because they are effective in treating breast cancer in some postmenopausal women. The presence of specific binding sites for gonadotropin-releasing hormone was demonstrated in human breast carcinomas by means of a novel approach of ligand immunoblotting. The results indicate a possible mechanism by which the peptide has direct effects on this tissue. These binding proteins were not detectable in non-neoplastic breast tissue.     

Concerted nonsyntenic allelic loss in human colorectal carcinoma

Familial polyposis coli (FPC) is caused by an autosomal dominant gene on chromosome 5, and it has been proposed that colorectal cancer in the general population arises from loss or inactivation of the FPC gene, analogous to recessive tumor genes in retinoblastoma and Wilms' tumor. Since allelic loss can be erroneously scored in nonhomogeneous samples, tumor cell populations were first microdissected from 24 colorectal carcinomas, an additional nine cancers were engrafted in nude mice, and nuclei were flow-sorted from an additional two. Of 31 cancers informative for chromosome 5 markers, only 6 (19%) showed loss of heterozygosity of chromosome 5 alleles, compared to 19 of 34 (56%) on chromosome 17, and 17 of 33 (52%) on chromosome 18. Therefore, it appears that (i) FPC is a true dominant for adenomatosis but not a common recessive gene for colon cancer; and (ii) simple Mendelian models involving loss of alleles at a single locus may be inappropriate for understanding common human solid tumors.     

Contribution of human alpha-defensin 1, 2, and 3 to the anti-HIV-1 activity of CD8 antiviral factor

It has been known since 1986 that CD8 T lymphocytes from certain HIV-1-infected individuals who are immunologically stable secrete a soluble factor, termed CAF, that suppresses HIV-1 replication. However, the identity of CAF remained elusive despite an extensive search. By means of a protein-chip technology, we identified a cluster of proteins that were secreted when CD8 T cells from long-term nonprogressors with HIV-1 infection were stimulated. These proteins were identified as alpha-defensin 1, 2, and 3 on the basis of specific antibody recognition and amino acid sequencing. CAF activity was eliminated or neutralized by an antibody specific for human alpha-defensins. Synthetic and purified preparations of alpha-defensins also inhibited the replication of HIV-1 isolates in vitro. Taken together, our results indicate that alpha-defensin 1, 2, and 3 collectively account for much of the anti-HIV-1 activity of CAF that is not attributable to beta-chemokines.     

人癌症/睾丸相关蛋白XAGE-1b原核表达载体的构建及融合蛋白的表达

目的构建人癌症/睾丸相关蛋白XAGE-1b原核表达载体及诱导XAGE-1融合蛋白表达。方法从文库质粒pACT2-XAGE-1b中利用PCR法扩增XAGE-b cDNA编码序列,将其克隆到pET-32a载体中,并将重组质粒pET-32bXAGE-1b转染大肠杆菌DE3中,用异丙基硫代半乳糖苷（IPTG）诱导表达,Western blot检测融合蛋白表达。结果原核表达载体pET-32a-XAGE-1b构建成功;转染菌株经IPTG诱导后,出现约29 kD蛋白过表达,Western-blot检测显示His6融合蛋白表达。结论成功构建原核表达载体pET-32a-XAGE-1b,转染菌株可表达His6融合蛋白。     

Detection of a cellular oncogene in spontaneous liver tumors of B6C3F1 mice

An active cellular oncogene was demonstrated in hepatocellular neoplasms arising spontaneously in 24-month-old B6C3F1 mice. DNA isolated from the tumorous tissue and transfected into NIH 3T3 cells showed an 82 percent (9 of 11 animals) frequency of foci induction. In contrast, DNA isolated from the surrounding nontumorous hepatic tissue from the same animals and DNA from other 24-month-old B6C3F1 mice without tumors did not cause transformation in the NIH 3T3 cell assay. This strain of mouse is used extensively in carcinogen bioassays, and the observed high frequency of transformation (82 percent, compared to 10 to 20 percent in humans) supports the concept that the B6C3F1 mouse is hypersusceptible to liver tumor development. It also emphasizes the need to further understand the mechanisms of oncogene activation in animals used for long-term studies of toxicity and oncogenicity before evaluating potential human risk.     

纳米碳示踪剂在cN0期甲状腺乳头状癌中央区淋巴结清扫术中的应用

目的 了解纳米碳示踪剂在cN0期甲状腺乳头状癌中央区淋巴结清扫术中应用效果.方法 100例cN0期甲状腺乳头状癌患者随机分为观察组和对照组,两组均行甲状腺全切除及中央组淋巴结清扫,观察组加用纳米碳示踪剂.比较两组手术情况、淋巴结清扫和转移数、血钙和甲状旁腺激素(PTH)水平、并发症.结果 观察组住院时间、术后2 d血钙...     

Physalaemin: an amphibian tachykinin in human lung small-cell carcinoma

Immunoreactivity to the amphibian peptide physalaemin was characterized from extracts of a human lung small-cell carcinoma by immunological, chemical, and pharmacological means. Tumor-related peptide cross-reacted with three antiserums to physalaemin to yield 1.1 to 1.6 nanomoles per gram of tissue. Physalaemin and tumor peptide had similar retention times on high-performance liquid chromatography after chemical and enzymic modifications that included pH changes, oxone oxidation, use of a hydrophilic ion-pairing reagent, and digestion with trypsin and pyroglutamate aminopeptidase. Both physalaemin and the tumor peptide produced a contractile response of isolated guinea pig ileum at threshold concentrations of approximately 100 to 150 picograms per milliliter. These data suggest that small-cell carcinoma of the lung contains a physalaemin-like peptide that has structural and biological homology to its amphibian counterpart.     

人大肠癌组织中nm23—H1表达及其与转移的关系

目的：探讨ｎｍ２３－Ｈ１基因表达与大肠癌转移的关系。方法：应用过氧化酶标记的链霉卵白素（ＳＰ）染色法对３３例正常大肠粘膜、１３４例癌旁粘膜及１９３便大肠癌免疫组织化学染色,并对染色结果进行观察,结果：大肠粘膜与癌旁粘膜间ｎｍ２３－Ｈ１表达阳性差异无显著性,但ｎｍ２３－Ｈ１在良、恶性大肠癌组织中的表达阳性率碾 显著性。ｎｍ２３－Ｈ１表达阳性率仅在正常、良性大肠组织与转移的大肠癌间差异有显著性,但与未