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Identification of substrate binding site of cyclin-dependent kinase 5

JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第14期274卷 9600-9606页

作者： Sharma, P Steinbach, PJ Sharma, M Amin, ND Barchi, JJ Pant, HC NINDS Neurochem Lab NIH Bethesda MD 20892 USA NINDS Ctr Mol Modeling Ctr Informat Technol NIH Bethesda MD 20892 USA NINDS Med Chem Lab NIH Bethesda MD 20892 USA

Cyclin-dependent kinase 5 (CDK5), unlike other CDKs, is active only in neuronal cells where its neuron-specific activator p35 is present. However, it phosphorylates serines/threonines in S/TPXK/R-type motifs Like other CDKs. The tail portion of neurofilament-H contains more than 50 KSP repeats, and CDK5 has been shown to phosphorylate S/T specifically only in KS/ TPXK motifs, indicating highly specific interactions in substrate recognition. CDKs have been shown to have a high preference for a basic residue (lysine or arginine) as the n+3 residue, n being the location in the primary sequence of a phosphoacceptor serine or threonine, Because of the lack of a crystal structure of a CDK-substrate complex, the structural basis for this specific interaction is unknown, me have used site-directed mutagenesis ("charged to alanine") and molecular modeling techniques to probe the recognition interactions for substrate peptide (PKTPKKAKKL) derived from histone H1 docked in the active site of CDK5, The experimental data and computer simulations suggest that Asp(86) and Asp(91) are key residues that interact with the lysines at positions n+2 and/or n+3 of the substrates.

关键词：氨基酸序列天冬酰胺/代谢结合部位 CDC2-CDC28激酶类计算机模拟细胞周期蛋白依赖激酶2 细胞周期蛋白依赖激酶5 细胞周期蛋白质依赖激酶类/化学细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白质依赖激酶类/代谢动力学分子序列数据诱变定点蛋白质构象蛋白质丝氨酸苏氨酸激酶/化学序列比对序列同源性氨基酸构效关系

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Initiation of human DNA replication in vitro using nuclei from cells arrested at an initiation-competent state

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13699-13707页

作者： Krude, T Univ Cambridge Wellcome CRC Inst Cambridge CB2 1QR England Univ Cambridge Dept Zool Cambridge CB2 3EJ England

Initiation of human DNA replication is investigated in vitro, using initiation-competent nuclei isolated from cells arrested in late G(1) phase by a 24-h treatment with 0.5 mM mimosine (Krude, T, (1999) Exp. Cell Res. 247, 148-159). Nuclei isolated from mimosine-arrested HeLa cells initiate semiconservative DNA replication upon incubation in cytosolic extracts from proliferating human cells. Initiation occurs in the absence and presence of a nuclear membrane. The cyclin-dependent kinase (Cdk) inhibitors roscovitine and olomoucine inhibit initiation of DNA replication, indicating a dependence of initiation on Cdk activity. Cell fractionation shows that cyclins A, E, and Cdk2 are bound to nuclei from mimosine-arrested cells. Exogenously added human cyclin A Cdk2 and cyclin E Cdk2 complexes, but not cyclin B1/Cdk1 or cyclin D2/Cdk6, can overcome inhibition of initiation by roscovitine in vitro. Depleting Cdk2 from cytosolic extract does not prevent initiation, demonstrating that cyclin Cdk2 complexes are not required in the soluble extract, but are provided by the nuclei. Initiation depends further on an essential and soluble activity present in cytosolic extracts from proliferating cells, but not from mimosine-arrested cells, acting together with nuclear cyclin/Cdk2 activity.

关键词： CDC2-CDC28激酶类细胞核/遗传学细胞周期蛋白依赖激酶2 细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白类/遗传学 DNA复制蛋白质丝氨酸苏氨酸激酶/遗传学人类

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The Elm1 kinase functions in a mitotic signaling network in budding yeast

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MOLECULAR AND CELLULAR BIOLOGY 1999年第12期19卷 7983-7994页

作者： Sreenivasan, A Kellogg, D Univ Calif Santa Cruz Dept Biol Sinsheimer Labs Santa Cruz CA 95064 USA

In budding yeast, the Clb2 mitotic cyclin initiates a signaling network that negatively regulates polar bud growth during mitosis. This signaling network appears to require the function of a Clb2-binding protein called Nap1, the Cdc42 GTPase, and two protein kinases called Gin4 and Cla4. In this study, we demonstrate that the Elm1 kinase also plays a role in the control of bud growth during mitosis. Cells carrying a deletion of the ELM1 gene undergo a prolonged mitotic delay, fail to negatively regulate polar bud growth during mitosis, and show defects in septin organization. In addition, Elm1 is required in vivo for the proper regulation of both the Cla4 and Gin4 kinases and interacts genetically with Cla4, Gin4, and the mitotic cyclins. Previous studies have suggested that Elm1 may function to negatively regulate the Swe1 kinase. To further understand the functional relationship between Elm1 and Swe1, we have characterized the phenotype of Delta elm1 Delta swe1 cells. We found that Delta elm1 Delta swe1 cells are inviable at 37 degrees C and that a large proportion of Delta elm1 Delta swe1 cells grown at 30 degrees C contain multiple nuclei, suggesting severe defects in cytokinesis. In addition, we found that Elm1 is required for the normal hyperphosphorylation of Swe1 during mitosis. We propose a model in which the Elm1 kinase functions in a mitotic signaling network that controls events required for normal bud growth and cytokinesis, while the Swe1 kinase functions in a checkpoint pathway that delays nuclear division in response to defects in these events.

关键词： CDC28蛋白激酶 S酿酒酵母/代谢细胞周期蛋白质类细胞周期蛋白B/代谢细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白质依赖激酶类/代谢细胞周期蛋白质依赖激酶类/生理学酶激活真菌蛋白质类/遗传学真菌蛋白质类/代谢真菌蛋白质类/生理学基因真菌有丝分裂诱变磷酰化蛋白质丝氨酸苏氨酸激酶/遗传学蛋白质丝氨酸苏氨酸激酶/代谢蛋白质丝氨酸苏氨酸激酶/生理学蛋白酪氨酸激酶类/遗传学蛋白酪氨酸激酶类/代谢酿酒酵母菌/酶学酿酒酵母菌/生长和发育酿酒酵母蛋白质类信号传导动物兔

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Aberrant expression of the cell cycle associated proteins TP53, MDM2, p21, p27, cdk4, cyclin D1, RB, and EGFR in cervical carcinomas

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GYNECOLOGIC ONCOLOGY 1999年第2期73卷 223-228页

作者： Skomedal, H Kristensen, GB Lie, AK Holm, R Univ Oslo Norwegian Radium Hosp Dept Pathol Inst Canc Res N-0310 Oslo Norway Univ Oslo Norwegian Radium Hosp Dept Gynecol Oncol Inst Canc Res N-0310 Oslo Norway

Objective, The aims of this study were to study aberrant expression and coexpression of the cell cycle associated proteins TP53, p21, p27, cyclin D1, cdk4, RE, EGFR, and MDM2 in cervical carcinomas, to correlate protein alterations with histopathological and clinical parameters, and to evaluate whether these alterations provide prognostic information. Methods, Seventy-four cervical carcinomas and 10 cases of normal cervical epithelium from patients with benign uterine leiomyomas were investigated immunohistochemically for aberrant expression of the cell cycle associated proteins using the biotin-streptavidin-peroxidase method and the OptiMax Plus automated cell staining system, Results. In normal cervical epithelium p27 immunostaining was identified in more than 50% of the cells, cdk4 in 5-50% of the cells, and EGFR in less than 5% of the cells, whereas no immunostaining for TP53, p21, MDM2, or cyclin D1 was detected. Positive RE protein staining was identified in all cases of normal cervical epithelium. RE protein staining was also identified in all carcinomas of the cervix uteri. Overexpression of p21 was found in 96% of the tumors, MDM2 in 35%, cdk4 in 69%, cyclin D1 in 3%, and EGFR in 20% of the tumors. A low level of p27 was observed in 65% of the cases. In a previous study, the TP53 protein level has been found to be elevated in 41 of the 74 (55%) cases included in this work. Significant coexpression was seen for TP53 and MDM2 (P = 0.001);concording results were observed in 67% of the cases. There was no difference in aberrant expression or coexpression of any of the cell cycle regulatory proteins related to histological type, grade of differentiation, FIGO stage, or relapse-free survival. Conclusion. The high number of cases showing increased levels of p21 and cdk4 and decreased levels of p27 suggests that these proteins may be important in the pathogenesis of cervical carcinoma. Furthermore aberrant expression of MDM2 in a smaller but significant fraction of

关键词：细胞周期蛋白质类/遗传学细胞周期蛋白D1/遗传学细胞周期蛋白依赖激酶4 细胞周期蛋白质依赖激酶类/遗传学基因表达调控肿瘤/遗传学微丝蛋白质类/遗传学肌蛋白质类肿瘤蛋白质类/遗传学核蛋白质类癌基因蛋白质p21(ras)/遗传学原癌基因蛋白质类/遗传学原癌基因蛋白质c-mdm2 受体表皮生长因子/遗传学视网膜母细胞瘤蛋白质/遗传学肿瘤抑制蛋白质p53/遗传学宫颈肿瘤/遗传学成年人老年人老年人 80以上女(雌)性人类中年人

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Myc downregulation by transforming growth factor β required for activation of the p15^Ink4b G₁ arrest pathway

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MOLECULAR AND CELLULAR BIOLOGY 1999年第9期19卷 5913-5922页

作者： Warner, BJ Blain, SW Seoane, J Massagué, J Mem Sloan Kettering Canc Ctr Cell Biol Program New York NY 10021 USA Mem Sloan Kettering Canc Ctr Howard Hughes Med Inst New York NY 10021 USA

The antimitogenic action of transforming growth factor beta (TGF-beta) in epithelial cells involves cyclin-dependent kinase (cdk) inhibitory gene responses and downregulation of c-Myc expression. Although the cdk inhibitory responses are sufficient for G(1) arrest, enforced expression of c-Myc prevents G(1) arrest by TGF-beta. We investigated the basis of this antagonism by using Mv1Lu lung epithelial cell lines that conditionally express levels of human c-Myc. We show that c-Myc prevents induction of the cdk4 inhibitor p15(Ink4b) and the subsequent inhibition of G(1) cdks by TGF-beta. We assessed the significance of this effect by analyzing the oligomeric state of cdk4 in these cells. In proliferating cells, endogenous cdk4 is distributed among three populations: an abundant high-molecular-mass (>400-kDa) pool of latent cdk4 that serves as a source of cdk4 for cyclin D, a low-abundance pool containing active cyclin D-cdk4 complexes, and an inactive population of monomeric cdk4. Cell stimulation with TGP-beta converts the latent and active cdk4 pools into inactive cdk4, an effect that is specifically mimicked by overexpression of p15 but not by other forms of G(1) arrest. This process of TGP-beta-induced cdk4 inactivation is completely blocked by expression of c-Myc, even though the latent and active cdk4 complexes from c-Myc-expressing cells remain sensitive to dissociation by p15 in vitro, c-Myc causes a small increase in cyclin D levels, but this effect contributes little to the loss of TGF-beta responses in these cells. The evidence suggests that c-Myc interferes with TGP-beta activation of the p15 G(1) arrest pathway. TGP-beta must therefore downregulate c-Myc in order to activate this pathway.

关键词：氨基酸序列碱基序列载体蛋白质类/遗传学载体蛋白质类/代谢细胞周期蛋白质类细胞系细胞周期蛋白D 细胞周期蛋白依赖激酶4 周期素依赖激酶抑制剂p15 周期素依赖激酶抑制剂p16 细胞周期蛋白质依赖激酶类/拮抗剂和抑制剂细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白质依赖激酶类/代谢细胞周期蛋白类/代谢 DNA/遗传学减量调节/药物作用酶抑制剂/代谢 G1期/药物作用 G1期/遗传学 G1期/生理学基因表达调控基因 myc/药物作用水貂分子序列数据启动区遗传原癌基因蛋白质类转化生长因子β/药理学肿瘤抑制蛋白质类动物人类

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p53 binds selectively to the 5′ untranslated region of cdk4, an RNA element necessary and sufficient for transforming growth factor β- and p53-mediated translational inhibition of cdk4

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MOLECULAR AND CELLULAR BIOLOGY 2000年第22期20卷 8420-8431页

作者： Miller, SJ Suthiphongchai, T Zambetti, GP Ewen, ME Dana Farber Canc Inst Boston MA 02115 USA Harvard Univ Sch Med Boston MA 02115 USA St Jude Childrens Res Hosp Dept Biochem Memphis TN 38105 USA

One consequence of transforming growth factor beta (TGF-beta) treatment is inhibition of Cdk4 synthesis, and this is dependent on p53. Here, we show that the 5' untranslated region (UTR) of the cdk4 mRNA is both necessary and sufficient for wild-type p53-dependent TGF-beta -regulated translational inhibition of cdk4. Wild-type p53 bound selectively to the 5' UTR of the cdk4 mRNA and inhibited translation of RNAs that contain this region. RNA binding and translational control are two genetically separable functions of p53, as are specific and nonspecific RNA binding. Moreover, transactivation-defective mutants of p53 retain the ability to regulate cdk4 translation. Our findings suggest that p53 functions as a regulator of translation in response to TGF-beta in vivo.

关键词： 5'非翻译区细胞周期蛋白依赖激酶4 细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白质依赖激酶类/代谢减量调节突变蛋白质生物合成原癌基因蛋白质类 RNA 未翻译/代谢转化生长因子β/代谢肿瘤抑制蛋白质p53/遗传学肿瘤抑制蛋白质p53/代谢动物

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The orphan receptor COUP-TFII regulates G2/M progression of breast cancer cells by modulating the expression/activity of p21^WAF1/CIP1, cyclin D1, and cdk2

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第3期270卷 1144-1153页

作者： Nakshatri, H Mendonca, MS Bhat-Nakshatri, P Patel, NM Goulet, RJ Cornetta, K Indiana Univ Sch Med Dept Surg Indianapolis IN 46202 USA Indiana Univ Sch Med Dept Biochem & Mol Biol Indianapolis IN 46202 USA Indiana Univ Sch Med Walther Oncol Ctr Indianapolis IN 46202 USA Indiana Univ Sch Med Dept Radiat Oncol Indianapolis IN 46202 USA Indiana Univ Sch Med Dept Med Indianapolis IN 46202 USA Indiana Univ Sch Med Dept Microbiol & Immunol Indianapolis IN 46202 USA Indiana Univ Sch Med Dept Med & Mol Genet Indianapolis IN 46202 USA

The orphan receptors COUP-TFI and COUP-TFII play an important role in development and differentiation by activating specific genes and by modulating the activity of nuclear receptors including estrogen receptor alpha (ER alpha) and retinoic acid receptors (RARs). Previously, it was demonstrated that the expression and activity of ER alpha and RARs are lost or impaired in anti-estrogen-resistant breast cancers. Here we show that, similar to ER alpha and RARs, the expression of COUP-TFII but not COUP-TFI is reduced in similar to 30% of breast cancer cell lines. introduction of COUP-TFII to MDA-MB-435 cells resulted in reduced growth and plating efficiency. Interestingly, COUP-TFII increased the expression of cyclin D1 and p21(WAF1/CIP1) in MDA-MB-435 cells. Although parental and COUP-TFII-transduced cells progressed through the G1-S phase at a similar rate, progression of COUP-TFII cells through the G2/M transition phase was delayed. The activity of cdk2 required for G2/M progression was reduced in COUP-TFII cells compared to parental cells. This property of COUP-TFII is distinct from that of ER alpha and RARs, which usually modulate the G1 phase of breast cancer cells. Furthermore, these results reveal an important physiological function of COUP-TFII, which correlates with its ability to induce gene expression rather than modulation of nuclear receptor activity. (C) 2000 Academic Press.

关键词：乳腺肿瘤/代谢乳腺肿瘤/病理学 CDC2-CDC28激酶类 COUP转录因子Ⅱ COUP转录因子类细胞周期/生理学细胞分裂细胞周期蛋白D1/遗传学细胞周期蛋白D1/代谢细胞周期蛋白依赖激酶2 周期素依赖激酶抑制剂p21 细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白质依赖激酶类/代谢细胞周期蛋白类/遗传学细胞周期蛋白类/代谢 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/代谢酶抑制剂/代谢 G2期基因表达调控肿瘤动力学有丝分裂蛋白质丝氨酸苏氨酸激酶/遗传学蛋白质丝氨酸苏氨酸激酶/代谢受体类固醇/代谢转录因子/遗传学转录因子/代谢肿瘤细胞培养的女(雌)性人类

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Crk1, a novel Cdc2-related protein kinase, is required for hyphal development and virulence in Candida albicans

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MOLECULAR AND CELLULAR BIOLOGY 2000年第23期20卷 8696-8708页

作者： Chen, JY Zhou, S Wang, Q Chen, X Pan, T Liu, HP Univ Calif Irvine Coll Med Dept Biol Chem Irvine CA 92697 USA Chinese Acad Sci Shanghai Inst Biochem State Key Lab Mol Biol Shanghai 200031 Peoples R China

Both mitogen-activated protein kinases and cyclin-dependent kinases play a role in hyphal development in Candida albicans. Using an oligonucleotide probe-based screen, we have isolated a new member of the Cdc2 kinase subfamily, designated Crk1 (Cdc2-related kinase). The protein sequence of Crk1 is most similar to those of Saccharomyces cerevisiae Sgv1 and human Pkl1/Cdk9. In S. cerevisiae, CRK1 suppresses some, but not all, of the defects associated with an sgv1 mutant. Deleting both copies of CRK1 in C. albicans slows growth slightly but leads to a profound defect in hyphal development under all conditions examined. crk1/crk1 mutants are impaired in the induction of hypha-specific genes and are avirulent in mice. Consistent with this, ectopic expression of the Crk1 kinase domain (CRK1N) promotes filamentous or invasive growth in S. cerevisiae and hyphal development in C. albicans. The activity of Crk1 in S. cerevisiae requires Flo8 but is independent of Ste12 and Phd1. Similarly, Crk1 promotes filamentation through a route independent of Cph1 and Efg1 in C. albicans. RAS1(V13) can also activate filamentation in a cph1/cph1 efg1/efg1 double mutant. Interestingly, CRK1N produces florid hyphae in ras1/ras1 strains, while RAS1(V13) generates feeble hyphae in crk1/crk1 strains.

关键词：氨基酸序列 CDC2蛋白激酶 CDC2-CDC28激酶类白色念珠菌/细胞学白色念珠菌/遗传学白色念珠菌/致病力细胞周期细胞分化克隆分子细胞周期蛋白质依赖激酶类/遗传学 DNA结合蛋白质类/代谢真菌蛋白质类/代谢基因缺失基因真菌小鼠近交ICR 丝裂原激活蛋白激酶类/代谢分子序列数据突变核蛋白质类信息素类/药理学酿酒酵母蛋白质类序列同源性氨基酸抑制遗传反式激活因子类/代谢转录因子动物男(雄)性小鼠

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Cdk4 activation is dependent on the subunit rearrangement in the complexes

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第1期267卷 388-393页

作者： Takahashi, H Menjo, M Kaneko, Y Ikeda, K Matsushime, H Nakanishi, M Nagoya City Univ Sch Med Dept Biochem Mizuho Ku Nagoya Aichi 4678601 Japan Nippon Roche Res Ctr Mol Oncol Grp Kamakura Kanagawa 247 Japan Natl Inst Longev Sci Dept Geriatr Res Aichi 474 Japan Yokohama City Univ Sch Med Dept Pediat Yokohama Kanagawa 237 Japan

Although several factors have been implicated in the regulation of Cdk4 activity, little is known regarding the contributions of cyclin-dependent kinase inhibitors (CKIs) in Cdk4 activation in the mid G1 phase. Using a mouse macrophage cell line (Bac1.2F5), we found that most of Cdk4 bound to p15 when cells were in a quiescent state. Following CSF-1 stimulation, Cdk4 bound to cyclin D1 and then to p21, concomitant with the dissociation of p15 from the complexes. The activation of Cdk4 correlated well with p21 binding to the complexes, and the majority of active Cdk4 complexes contained p21, During regeneration of mouse liver after partial hepatectomy, Cdk4 activity coincided precisely with ternary complex formation of cyclin D1/Cdk4/p21. Using the baculovirus expression system, we succeeded in reconstituting a capacity for Cdk4 activation in insect cells, forming an active cyclin D1/Cdk4/p21 ternary complex. Taken together, it is suggested that p21 and cyclin D1 act cooperatively as activators of Cdk4 through the release of CKIs of the INK4 family. (C) 2000 Academic Press.

关键词：细胞周期/生理学细胞系细胞周期蛋白依赖激酶4 周期素依赖激酶抑制剂p21 细胞周期蛋白质依赖激酶类/化学细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白质依赖激酶类/代谢细胞周期蛋白类/代谢酶激活肝切除术肝/细胞学肝/生理学肝再生/生理学大分子物质巨噬细胞集落刺激因子/药理学巨噬细胞/细胞学小鼠近交BALBC 蛋白质结构三级原癌基因蛋白质类重组蛋白质类/代谢斜纹夜蛾属转染动物男(雄)性小鼠

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Targeted disruption of CDK4 delays cell cycle entry with enhanced p27^Kip1 activity

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MOLECULAR AND CELLULAR BIOLOGY 1999年第10期19卷 7011-7019页

作者： Tsutsui, T Hesabi, B Moons, DS Pandolfi, PP Hansel, KS Koff, A Kiyokawa, H Univ Illinois Coll Med Dept Mol Genet Chicago IL 60607 USA Univ Illinois Coll Med Ctr Canc Div Dev Therapeut Chicago IL 60607 USA Mem Sloan Kettering Canc Ctr Dept Human Genet New York NY 10021 USA Mem Sloan Kettering Canc Ctr Program Mol Biol New York NY 10021 USA

The mechanism by which cyclin-dependent kinase 4 (CDK4) regulates cell cycle progression is not entirely clear. Cyclin D/CDK4 appears to initiate phosphorylation of retinoblastoma protein (Rb) leading to inactivation of the S-phase-inhibitory action of Rb. However, cyclin D/CDK4 has been postulated to act in a noncatalytic manner to regulate the cyclin E/CDK2-inhibitory activity of p27(Kip1) by sequestration. In this study we investigated the roles of CDK4 in cell cycle regulation by targeted disruption of the mouse CDK4 gene. CDK4(-/-) mice survived embryogenesis and showed growth retardation and reproductive dysfunction associated with hypoplastic seminiferous tubules in the testis and perturbed corpus luteum formation in the ovary. These phenotypes appear to be opposite to those of p27-deficient mice such as gigantism and gonadal hyperplasia. A majority of CDK4(-/-) mice developed diabetes mellitus by 6 weeks, associated with degeneration of pancreatic islets. Fibroblasts from CDK4(-/-) mouse embryos proliferated similarly to wild-type embryonic fibroblasts under conditions that promote continuous growth. However, quiescent CDK4(-/-) fibroblasts exhibited a substantial (similar to 6-h) delay in S-phase entry after serum stimulation. This cell cycle perturbation by CDK4 disruption was associated with increased binding of p27 to cyclin E/CDK2 and diminished activation of CDK2 accompanied by impaired Rb phosphorylation. Importantly, fibroblasts from CDK4(-/-) p27(-/-) embryos displayed partially restored kinetics of the G(0)-S transition, indicating the significance of the sequestration of p27 by CDK-4. These results suggest that at least part of CDK4's participation in the rate-limiting mechanism for the G(0)-S transition consists of controlling p27 activity.

关键词：萎缩细胞周期/遗传学细胞周期蛋白质类黄体/病理学细胞周期蛋白依赖激酶4 细胞周期蛋白依赖激酶6 周期素依赖激酶抑制剂p27 细胞周期蛋白质依赖激酶类/遗传学细胞周期蛋白质依赖激酶类/代谢糖尿病糖尿纯合子小鼠突变型微管相关蛋白质类/遗传学微管相关蛋白质类/代谢蛋白质结合蛋白质丝氨酸苏氨酸激酶/分析原癌基因蛋白质类细精管/病理学组织分布肿瘤抑制蛋白质类动物女(雌)性男(雄)性小鼠

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