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    Proceedings of the National Academy of Sciences of the United States of America

  • 中文名称: 美利坚合众国国家科学院院刊
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  • ISSN: 0027-8424
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352条结果
  • 机译 脊髓背柱白质中的神经元:复杂的神经纤维位于意外位置
    摘要:It is common to think of gray mattcr as the site of integration in neural circuits and white matter as the wires that conncct different groups of neurons. The dorsal column (DC) white matter, for example, is the spinal cord axonal pathway through which a topographic map of the body is conveyed to the somatosensory cortex. We now describe a network of neurous located along the midline of the DCs. The neurons are present in several mammals, including primates and birds, and have a profuse dendritic arbor that expresses both the neuron-specific marker, mi- crotuhule-associated protein-2, and the neurokinin-1 recep- tor, a target of the neuropeptide, substance P. Electron microscopy and double immunostaining for synaptophysin and a marker of #gamma#-aminobutyric acid-ergic terminals doc- umented a rich synaptic input to these neurons. Finally, injection of a #gamma#-aminobulyric acid type A receptor antago- nist or of substance P into the cerebrospinal fluid of the rat spinal cord induced Fos expression and internalization of the neurokinin-1 receptor in these neurons, respectively, indicating that the DC neurons are under tonic inhibitory control and can respond to neurotransmitters that circulate in the cerebrospinal fluid.
  • 机译 胡为什么在哪里?早期响应基因信使RNA亚群的穿梭
    • 作者:Jack D. Keene;
    • 刊名:Proceedings of the National Academy of Sciences of the United States of America
    • 1999年第1期
    摘要:
  • 机译 基因治疗后在重度联合免疫缺陷小鼠模型中的病毒特异性免疫
    摘要:Human severe combined immunodeficiency (SCID) can be caused by defects in Janus kinase 3 (JAK3)- dependent cytokine signaling pathways. As a result, patients are at high risk of life-threatening infection. A JAK3 -/- SCID mouse model for the human disease has been used to test whetber transplant with retrovirally transduced bone marrow (BM) cells (JAK3 BMT) could restore immunity to an influ- enza A virus. The immune responses also were compared directly with those for mice transplanted with wild-type BM ( + / + BMT). After infection, approximately 90 of the JAK3 BMT or +/+ BMT mice survived, whereas all of the JAK3 -/- mice died within 29 days. Normal levels of influenza- specific IgG were present in plasma from JAK3 BMT mice at 14 days after respiratory challenge, indicating restoration of B cell function. Influenza-specific CD4+ and CD8+ T cells were detected in the spleen and lymph nodes, and virus- specific CD8+ effectors localized to the lungs of the JAK3 BMT mice. The kinetics of the specific host response corre- lated with complete clearance of the virus within 2 weeks of the initial exposure. By contrast, the JAK3 -/- mice did not show any evidence of viral immunity and were unable to control this viral pneumonia. Retroviral-mediated JAK3 gene transfer thus restores diverse aspects of cellular and humoral immunity and has obvious potential for human autologous BMT.
  • 机译 重组杆状病毒载体转导的哺乳动物细胞中的瞬时稳定基因表达
    摘要:Recombinant baculoviruses can serve as gene-transfer vehicles for transient expression of recombinant proteins in a wide range of mammalian cell types. Further- more, by inclusion of a dominant selectable marker in the viral vector, cell lines can be derived that stably express recombi- nant genes. A virus was constructed containing two expression cassettes controlled by constitutive mammalian promoters: the cytomegalovirus immediate early promoter/enhancer di- recting expression of green fluorescent protein and the simian virus 40 (SV40) early promoter controlling neomycin phos- photransferase II. Using this virus, efficient gene delivery and expression was observed and measured in numerous cell types of human, primate, and rodent origin. In addition to com- monly used transformed cell lines such as HeLa, CHO, Cos-7, and 293, this list includes primary human keratinocytes and bone marrow fibroblasts. In all cases, addition of butyrate or trichostatin A (a selective histone deacetylase inhibitor) to transduced cells markedly enhanced the levels of reportcr protein expression observed. When transduced cells are put under selection with the antibiotic G418, cell lines can be obtained at high frequency that stably maintain the expres- sion cassettes of the vector DNA and exhibit stable, high-level expression of the reporter gene. Stably transduced derivatives have been selected from a substantial number of different cell types, suggesting that stable lines can be derived from any cell type that exhibits transient expression.
  • 机译 使用靶向细胞核的富含硼的低聚磷酸二酯进行癌症治疗
    摘要:The viability of boron neutron capture ther- apy depends on the development of tumor-targeting agents that contain large numbers of boron-10 (~10B) atoms and are readily taken up by cells. Here we report on the selective uptake of homogeneous fluorescein-labeled nido-carboranyl oligomeric phosphate diesters (nido-OPDs) by the cell nucleus and their long-term retention after their delivery into the cytoplasm of TC7 cells by microinjection. All nido-OPDs accumulated in the cell nucleus within 2 h after microinjec- tion. However, nido-OPDs in which the carborane cage was located on a side chain attached to the oligomeric backbone were redistributed between both the cytoplasm and nucleus after 24 h of incubation, whereas nido-OPDs in which the carborane cage was located along the oligomeric backbone remained primarily in the nucleus. Furthermore, cell-free incubation of digitonin-permeabilized TC7 cells with the nido-OPDs resulted in nuclear accumulation of the com- pounds, thus corroborating the microinjection studies. Our observation of fluorescence primarily located in the cell nucleus indicates that nuclear-specific uptake of sufficient amounts of ~10B for effective boron neutron capture therapy (approx=10~8-1O~9, ~10B atoms/tumor cell) via nido-OPDs is achievable.
  • 机译 电压敏感的Lc型Ca〜2 +通道在功能上与胞吐机制耦合
    • 作者:OFER WISER; ANA HERNANDEZ;
    • 刊名:Proceedings of the National Academy of Sciences of the United States of America
    • 1999年第1期
    摘要:Although N- and P-type Ca~2+ channels pre- dominant in fast-secreting systems, Lc-type Ca~2+ channels (C-class) can play a similar role in certain secretory cells and synapses. For example, in retinal bipolar cells, Ca~2+ entry through the Lc channels triggers ultrafast exocytosis, and in pancreatic #beta#-cells, evoked secretion is highly sensitive to Ca~2+. These findings suggest that a rapidly release pool of vesicles colocalizes with the Ca~2+ channels to allow high Ca~2+ con- centration and a tight coupling of the Lc channels at the release site. In binding studies, we show that the Lc channel is physically associated with synaptotagmin (p65) and the soluble N-ethylmaleimide-sensitive attachment proteins re- ceptors: syntaxin and synaptosomal-associated protein of 25 kDa. Soluble N-ethylmaleimide-sensitive attachent proteins receptors coexpressed in Xenopus oocytes along with the Lc channel modify the kinetic properties of the channel. The modulatory action of syntaxin can be overcome by coexpress- ing p65, where at a certain ratio of p65/syntaxin, the channel regains its unaltered kinetic parameters. The cytosolic region of the channel, Lc_(753-893), separating repeats II-III of its #ALPHA#1C subunit, interacts with p65 and "pulls" down native p65 from rat brain membranes. Lc_(753-893) injected into single insulin- secreting #beta#-cell, inhibits secretion in response to channel opening, but not in response to photolysis of caged Ca~2+, nor does it affect Ca~2+ current. These results suggest that Lc_(753-893) competes with the endogenous channel for the synaptic pro-
  • 机译 单个#alpha#颗粒穿过哺乳动物细胞核的致癌转化潜能
    摘要:Domestic, low-level exposure to radon gas is considered a major environmental lung-cancer hazard involv- ing DNA damage to bronchial cells by #alpha# particles from radon progeny. At domestic exposure levels, the relevant bronchial cells are very rarely traversed by more than one a particle, whereas at higher radon levels-at which epidemiological studies in uranium miners allow lung-cancer risks to be quantified with reasonabl. precision-these bronchial cells are frequently exposed to multiple #alpha#-particle traversals. Mea- suring the oncogenic transforming effects of exactly one #alpha# particle without the confounding effects of multiple traversals has hitherto been unfeasible, resulting in uncertainty in extrapolations of risk from high to domestic radon levels. A technique to assess the effects of single #alpha# particles uses a charged-particle microbeam, which irradiates individual cells or cell nuclei with predefined exact numbers of particles. Although previously too slow to assess the relevant small oncogenic risks, recent improvements in throughput now permit microheam irradiation of large cell numhers, allowing the first oncogenic risk measurements for the traversal of exactly one a particle through a cell nncleus. Given positive controls to ensure that the dosimetry and biological controls were comparable, the measured oncogenicity from exactly one a particle was significantly lower than for a Poisson- distributed mean of one #alpha# particle, implying that cells tra- versed by multiple #alpha# particles contribute most of the risk. If this result applies ge
  • 机译 番茄的侧向抑制基因(Ls)编码VHIID蛋白家族的新成员
    摘要:The ability of the shoot apical meristem to multiply and distribute its meristematic potential through the formation of axillary meristems is essential for the diversity of forms and growth habits of higher plants. In the tateral suppressor mutant of tomato the initiation of axillary meris- tems is prevented, thus offering the unique opportunity to study the molecular mechanisms underlying this important function of the shoot apical meristem. We report here the isolation of the Lateral suppressor gene by positional cloning and show that the mutant phenotype is caused by a complete loss of function of a new member of the VHIID family of plant regulatory proteins.
  • 机译 BCR-ABL癌蛋白可能与干皮色素B组蛋白相互作用
    摘要:The previously uncharacterized CDC24 ho- mology domain of BCR, which is missing in the P185 BCR- ABL oncogene of Philadelphia chromosome (Ph1)-positive acute lymphocytic leukemia but is retained in P21O BCR-ABL of chronic myelogeneous leukemia, was found to bind to the xeroderma pigmentosum group B protein (XPB). The binding appeared to be required for XPB to be tyrosine-phosphory- lated by BCR-ABL. The interaction not only reduced both the ATPase and the helicase activities of XPB purified in the baculovirus system but also impaired XPB-mediated cross- complementation of the repair deficiency in rodent UV- sensitive mutants of group 3. The persistent dysfunction of XPB may in part underlie genomic instability in blastic crisis.
  • 机译 环氧合酶(COX)-2的系统生物合成前列环素:一种选择性抑制剂COX-2的人药理作用
    • 作者:B. F. MCADAM; I.A. MARDINI;
    • 刊名:Proceedings of the National Academy of Sciences of the United States of America
    • 1999年第1期
    摘要:Prostaglandins (PG) are synthesized by two isoforms of the enzyme PG G/H synthase [cyclooxygenase (COX)]. To examine selectivity of tolerated doses of an inhibitor of the inducible COX-2 in humans, we examined the effects of celecoxib on indices of COX-1-dependent platelet thromboxane (Tx) A_2 and on systemic biosynthesis of pros- tacyclin in vivo. Volunteers received doses of 100, 400, or 800 mg of celecoxib or 800 mg of a nonselective inhibitor, ibupro- fen. Ibuprofen, but not celecoxib, significantly inhibited TxA_2- dependent aggregation, induced ex vivo by arachidonic acid (83 +- 11 vs. 11.9 +- 2.2, P < 0.005) and by collagen. Neither agent altered aggregatiou induced by thromboxane mimetic, U46619. Ibuprofen reduced serum TxB-2(-95 +- 2 vs. -6.9 +- 4.2; P < 0.001) and urinary excretion of the major Tx metabOlite, 11-dehydro TxB_2 (-70 +- 9.9 vs. -20.3 +- 5.3; P < 0.05) when compared with placebo. Despite a failure to suppress TxA_2-dependant platelet aggregation, celecoxib had a modest but significant inhibitory effect on serum TxB_2 4 hr after dosing. By contrast, both ibuprofen and celecoxib sup- pressed a biochemical index of COX-2 activity (endotoxin induced PGE_2 in whole blood ex vivo) to a comparable degree (-93.3 +- 2 vs. -83 +- 6.1). There was no significant difference between the doses of celecoxib on COX-2 inhibition. Celecoxib and ibuprofen suppressed urinary excretion of the prostacyclin metabolite 2,3 dinor 6-keto PGF_(1#alpha#). These data suggest that (i) platelet COX-1-dependent aggregation is not inhibited by up to 800 mg of celecoxib; (ii) c
  • 机译 缺乏肌营养不良蛋白和MyoD的小鼠的严重心肌病
    摘要:The mdx mouse, a mouse model of Duchenne muscular dystrophy, carries a loss-of-function mutatiou in dystrophin, a component of the membrane-associated dystro- phin-glycoprotein complex. Unlike humans, mdx mice rarely display cardiac abnormalities and exhibit dystrophic changes only in a small number of heavily used skeletal muscle groups. By contrast, mdx:MyoD~(-/-) mice lacking dystrophin and the skeletal muscle-specific bHLH transcription factor MyoD display a severe skeletal myopathy leading to widespread dystrophic changes in skeletal muscle and premature death around 1 year of age. The severely increased phenotype of mdx:MyoD~(-/-) muscle is a consequence of impaired muscle regeneration caused by enhanced satellite cell self-renewal. Here we report that mdx:MyoD~(-/-) mice developed a severe cardiac myopathy with areas of necrosis associated with hypertrophied myocytes. Moreover, heart tissue from mdx:MyoD~(-/-) mice exhibited constitutive activation of stress- activated signaling components, similar to in vitro models of cardiac myocyte adaptation. Taken together, these results support the hypothesis that the progression of skeletal muscle damage is a significant contributing factor leading to devel- opment of cardiomyopathy.
  • 机译 质子从大肠杆菌的血红铜氧化酶中退出
    • 作者:ANNE PUUSTINEN;
    • 刊名:Proceedings of the National Academy of Sciences of the United States of America
    • 1999年第1期
    摘要:Pathways of proton entry have been identi- fied in the proton-translocating heme-copper oxidases, but the proton exit pathway is unknown. Here we report experi- ments with cytochrome bo_3 in Escherichia coli cells that may identify the beginning of the exit pathway. Systematic muta- tions of arginines 438 and 439 (R481 and R482 in the E. coli enzyme), numbering as in cytochrome aa_3 from bovine heart mitochondria, which interact with the ring D propionates of the two heme groups, reveal that the D propionate of the oxygen-binding heme is involved in proton pumping; its anionic form must be stabilized in ordcr for proton translo- cation to occur. This may locate the beginning of the pathway by which pumped protons exit from the enzyme structure.
  • 机译 果蝇秀丽隐杆线虫CED-4蛋白的促凋亡活性:caspase激活的相关机制。
    摘要:CED-4 protein plays an important role in the induction of programmed cell death in elegans through the activation of caspases. However, the precise mech- anisms by which it activates caspases remain unknown. To investigate the conservation of CED-4 function in evolution, transgenic Drosophifo lines that express CED-4 in the compound eye were generated. Ectopic expression of CED-4 in the eyes induced massive apoptotic cell death through caspase activation. An ATP-binding site (P-loop) mutation in CED-4 (K165R) causes a loss of function in its ability to activate Drosophila taspase, and an ATPase inhibitor blocks the CED-4-dependent caspase activity in Drosophila S2 cells. Immunoprecipitation analysis showed that both CED-4 and CED-4 (K165R) bind directly to Drosophila caspase drICE, and the overexpression of CED-4 (K165R) inhibits CED-4-, ecdysone-, or cycloheximide- dependent caspase activation in S2 cells. Furthermore, CED-4 (Kl65R) partially prevented cell death induced by CED-4 in Drosophila compound eyes. Thus, CED-4 function is evolution- arily conserved in Drosophila, and the molecular mechanisms by which CED-4 activates caspases might require ATP binding and direct interaction with the caspases.
  • 机译 聚谷氨酰胺介导的秀丽隐杆线虫感觉神经元的功能障碍和凋亡性死亡
    摘要:The effect of expressing human huntingtin fragments containing polyglutamine (polyQ) tracts of varying lengths was assessed in Caenorhobditis elegans ASH sensory neurons in young and old animals. Expression of a huntingtin fragment containing a polyQ tract of 150 residues (Htn-Q150) led to progressive ASH neurodegeneration but did not cause cell death. Progressive cell death and enhanced neurodegen- eration were observed in ASH neurons that coexpressed Htn-Q150 and a subthreshold dose of a toxic OSM-10::green fluorescent protein (OSM-10::GFP) fusion protein. Htn-Q150 huntingtin protein fragments formed protein aggregates in ASH neurons, and the number of ASH neurons containing aggregates increased as animals aged. ASH neuronal cell death required ced-3 caspase function, indicating that the observed cell death is apoptotic. Of interest, ced-3 played a critical role in Htn-Q150-mediated neurodegeneration but not in OSM1O::GFP-mediated ASH neurodegeneration. ced-3 function was important but not essential for the formation of protein aggregates. Finally, behavioral assays indicated that ASR neurons, coexpressing Htn-Q 150 and OSM1O::GFP, were functionally impaired at 3 days before the detection of neu- rodegeneration, cell death, and protein aggregates.
  • 机译 鼠气单胞菌[(24Z)-ethylidenelanost-8-en-3#beta#-ol],一种在机会病原体人类卡氏肺孢子虫中检出的稀有固醇:结构特征和化学合成
    摘要:Pneumocystis carinii pneumonia (PcP) remains among the most prevalent opportunstic infections among AIDS patients. Currently, drugs used clinically for deep mycosis act by binding ergosterol or disrupting its biosynthesis. Although clas- sified as a fungus, P. carinii lacks ergosterol. Instead, the pathogen synthesizes a number of distinct #DELTA#~7, 24-alkylsterols, despite the abundance of cholesterol, which it can scavenge from the lung alveolus. Thus, the pathogen-specific sterols appear vital for organism survival and proliferation. In the present study, high concentrations of a C_32 sterol were found in human- derived P. carinii hominis. The definitive structural identities of two C-24 alkylated lanosterol compounds, previously not re- ported for rat-derived P. carinii carinii, were determined by using GLC, MS, and NMR spectroscopy together with the chemical syntheses of authentic standards. The C_31 and C_32 sterols were identified as euphorbol (24-methylenelanost-8-en-3#beta#-ol) and pneumocysterol [(24Z)-ethylidenelanost-8-en-3#beta#- respec- tively. The identification of these and other 24-alkylsterols in P. carinii hominis suggests that (i) sterol C-24 methyltransferase activities are ertraoedinarily high in this organism, (ii) 24- alkysterols are important components of the pathogen's mem- branes, because the addition of these side groups onto the sterol sids cbain requires substantial ATP equivalents, and (iii) the inefficacy of azole drugs against P. carinii can be explained by the ability of this organism to form 24-alkysterols before demethyl- ation of the
  • 机译 Wnt信号的核终点:反式激活淋巴增强因子1诱导的肿瘤转化
    • 作者:MASAHIRO AOKI; ULRICH KRUSE;
    • 刊名:Proceedings of the National Academy of Sciences of the United States of America
    • 1999年第1期
    摘要:The interaction between #beta#-catenin and LEF- l/TCF transcription factors plays a pivotal role in the Wnt-1 signaling pathway. The level of #beta#-catenin is regulated by partner froteins, including glycogen synthase kinase-3#beta# (GSK-3#beta#) and the adenomatous polyposis coli (APC) tumor suppressor protein. Genetic defects in APC are responsible for a heritable predis- position to colon cancer. APC protein and GSK-3#beta# bind #beta#-cate- nui, retain it in the cytoplasm, and facilitate the proteolytic degradation of #beta#-catenin. Abrogation of this negative regulation allows #beta#-catenin to translocate to the nucleus and to form a transcriptional activator complex with the DNA-binding protein lymphoid-enhancing factor 1 (LEF-1). This complex is thought to be involved in tumorigenesis. Here we show that covalent linkage of LEF-1 to #beta#-catenin and to transcriptional activation domains derived from the estrogen receptor or the herpes simplex virns protein VP16 genenates transcriptional regulators that induce oncogenic transformation of chicken embryo fibroblasts. The chimeras between LEF-1 and #beta#-catenin or VP16 are constitu- tively active, whereas fusions of LEF-1 to the estrogen receptor are regulatable by estrogen. These experiments document the oncogenicity of transactivating LEF-1 and show that the trans- activation domain normally provided by #beta#-catenin can be re- placed by heterologous activation domains. These results suggest that the transactivating function of the LEF-1/#beta#-catenin com- plex is critical for tumorigenesis and that this compl
  • 机译 通过非侵入性神经营养蛋白递送至大脑进行神经保护
    • 作者:DAFANG WU;
    • 刊名:Proceedings of the National Academy of Sciences of the United States of America
    • 1999年第1期
    摘要:Brain-derived neurotrophic factor (BDNF) is neuroprotective in the ischemic hippocampus if the neuro- trophin is injected directly into the brain. However, the efficacy of BDNF via peripheral (i.v.) administration is lim- ited by the lack of transport of the neurotrophin through the brain capillary wall, which makes up the blood-brain barrier (BBB) in vivo. The present studies describe a molecular reformulation of BDNF that incorporates polyethylene glycol (PEG) moieties at surface carboxyl residues, to optimize plasma pharmacokinetics, and links pegylated BDNF to the OX26 mAb, which undergoes receptor-mediated transport through the BBB via the brain capillary endothelial trans- ferrin receptor. The BDNF-PEG 2000-biotin conjugated to OX26/streptavidin was administered i.v. daily to rats for 1 week after a 12-min period of transient forebrain ischemia. The neuronal density in the CA1 sector of the hippocampus was decreased 68 +- 10 at 1 week after the ischemia. There was no neuroprotective effect of the unconjugated BDNF or unconjugated OX26 mAb. However, the hippocampal CA1 neuronal density was normalized by i.v. administration of the BDNF-PEG 2000-biotin conjugated to OX26/streptavidin. These studies demonstrate that peripherally administered BDNF may have neuroprotective effects in brain, if the neurotrophin is reformulated to (i) optimize plasma pharma- cokinetics with carboxyl-directed pegylation, and (ii) enable transport tbrough the BBB by coupling to brain transport vectors.
  • 机译 选择性消除活化转录的介体蛋白突变
    摘要:Deletion of any one of three subunits of the yeast Mediator of transcriptional regulation, Med2, Pgdl (Hrsl), and Sin4, abolished activation by Gal4-VP16 in vitro. By contrast, other Mediator functions, stimulation of basal transcription and of TFIIH kinase activity, were unaffected. A different but overlapping Mediator subunit dependence was found for activation by Gcn4. The genetic requirements for activation in vivo were closely coincident with those in vitro. A whole genome expression profile of a #DELTA#med2 strain showed diminished transcription of a subset of inducible genes but only minor effects on "basal" transcription. These findings make an important connection between transcriptional acti- vation in vitro and in vivo, and identify Mediator as a "global" transcriptional coactivator.
  • 机译 从菜豆中分离出编码玉米醇溶蛋白O-葡萄糖基转移酶的细胞分裂素基因ZOG1
    摘要:Zeatin is the most active and ubiquitous of the naturally occurring cytokinins. The O-glucoside of zeatin, found in all plants examined, is considered to be important in cytokinin transport, storage, and protection against cytokinin oxidases. The enzyme UDPglucose:zeatin O-glucosyltrans- ferase (EC 2.4.1.203) was previously isolated from Phoseolus lunatus seeds. Immunoscreening of an expression library with monospecific antibody resulted in the isolation of a cDNA encoding the enzyme. The recombinant protein efficiently converts labeled zeatin to O-glucosylzeatin and has properties similar to the native enzyme. The cDNA of 1.5 kb contains an ORF encoding a 51.4-kDa polypeptide of 459 amino acids. The sequence is unique based on a BLAST search of data bases. The genomic scquence, isolated with PCR using specific primers based on the cDNA sequence, does not contain introns. The cloning of this gene provides the tools for further study of the regulation of cytokinin metabolism and analysis of the precise role of O-glucosylzeatin in plant development.
  • 机译 控制拟南芥不依赖于施肥的种子发育的基因
    • 作者:MING LUO; ANNA KOLTUNOW;
    • 刊名:Proceedings of the National Academy of Sciences of the United States of America
    • 1999年第1期
    摘要:We have cloned two genes, FIS1 and FIS2, that control both fertilization independent seed development and postpollination embryo development in Arabidopsis. These genes confer female gametophytic phenotypes. FIS2 encodes a protein with a C_2H_2 zinc-finger motif and three putative nuclear localization signals, indicating that it is likely to be a transcription factor. FIS1 encodes a protein with homology to the Drosophila Polycomb group gene Enhancer-of-zeste and is identical to the recently described Arabidopsis gene MEDEA FIS1 is a protein with a number of putative functional domains, including the SET domain present in Enhancer-of- zeste-related proteins. Comparison of the position of the lesions in the fis1 and medea mutant alleles indicates that fis1 is a null allele producing a truncated polypeptide lacking all the protein domains whereas the deduced protein from medea lacks only the SET domain. We present a model of the role of FIS1 and FIS2 gene products in seed development.
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