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101.
Castro Gabriel Vaisam Latorre Ana Frederica Sutter Korndorfer Fabíola Pozza de Carlos Back Lia Kubelka Lofgren Sara Emelie 《Biochemical genetics》2021,59(6):1666-1679
Biochemical Genetics - Obesity and overweight are worldwide public health problems with an evident genetic predisposition that is still poorly understood. In addition, great variability has been... 相似文献
102.
Anaya-Ramos Laura Díaz-Ruíz Araceli Ríos Camilo Mendez-Armenta Marisela Montes Sergio Aguirre-Vidal Yoshajandith García-Jiménez Sara Baron-Flores Veronica Monroy-Noyola Antonio 《Biometals》2021,34(6):1295-1311
BioMetals - Thallium (TI) is one of the most toxic heavy metals. Human exposure to Tl occurs through contaminated drinking water and from there to food, a threat to health. Recently, environmental... 相似文献
103.
Sara Ferluga Roy Hantgan Yehuda Goldgur Juha P. Himanen Dimitar B. Nikolov Waldemar Debinski 《The Journal of biological chemistry》2013,288(25):18448-18457
The EphA2 receptor tyrosine kinase is overexpressed in a number of malignancies and is activated by ephrin ligands, most commonly by ephrin-A1. The crystal structure of the ligand-receptor complex revealed a glycosylation on the Asn-26 of ephrin-A1. Here we report for the first time the significance of the glycosylation in the biology of EphA2 and ephrin-A1. Ephrin-A1 was enzymatically deglycosylated, and its activity was evaluated in several assays using glioblastoma (GBM) cells and recombinant EphA2. We found that deglycosylated ephrin-A1 does not efficiently induce EphA2 receptor internalization and degradation, and does not activate the downstream signaling pathways involved in cell migration and proliferation. Data obtained by surface plasmon resonance confirms that deglycosylated ephrin-A1 does not bind EphA2 with high affinity. Mutations in the glycosylation site on ephrin-A1 result in protein aggregation and mislocalization. Analysis of Eph/ephrin crystal structures reveals an interaction between the ligand''s carbohydrates and two residues of EphA2: Asp-78 and Lys-136. These findings suggest that the glycosylation on ephrin-A1 plays a critical role in the binding and activation of the EphA2 receptor. 相似文献
104.
105.
Bikash R. Pattnaik Sara Tokarz Matti P. Asuma Tyler Schroeder Anil Sharma Julie C. Mitchell Albert O. Edwards De-Ann M. Pillers 《PloS one》2013,8(8)
Snowflake Vitreoretinal Degeneration (SVD) is associated with the R162W mutation of the Kir7.1 inwardly-rectifying potassium channel. Kir7.1 is found at the apical membrane of Retinal Pigment Epithelial (RPE) cells, adjacent to the photoreceptor neurons. The SVD phenotype ranges from RPE degeneration to an abnormal b-wave to a liquid vitreous. We sought to determine how this mutation alters the structure and function of the human Kir7.1 channel. In this study, we expressed a Kir7.1 construct with the R162W mutation in CHO cells to evaluate function of the ion channel. Compared to the wild-type protein, the mutant protein exhibited a non-functional Kir channel that resulted in depolarization of the resting membrane potential. Upon co-expression with wild-type Kir7.1, R162W mutant showed a reduction of IKir7.1 and positive shift in ‘0’ current potential. Homology modeling based on the structure of a bacterial Kir channel protein suggested that the effect of R162W mutation is a result of loss of hydrogen bonding by the regulatory lipid binding domain of the cytoplasmic structure. 相似文献
106.
Mayank Singh Clayton R. Hunt Raj K. Pandita Rakesh Kumar Chin-Rang Yang Nobuo Horikoshi Robert Bachoo Sara Serag Michael D. Story Jerry W. Shay Simon N. Powell Arun Gupta Jessie Jeffery Shruti Pandita Benjamin P. C. Chen Dorothee Deckbar Markus L?brich Qin Yang Kum Kum Khanna Howard J. Worman Tej K. Pandita 《Molecular and cellular biology》2013,33(16):3390
107.
108.
Ailec Ho‐Plagaro Concepcin Santiago‐Fernandez Cristina Rodríguez‐Díaz Carlos Lopez‐Gmez Sara Garcia‐Serrano Francisca Rodríguez‐Pacheco Sergio Valdes Alberto Rodríguez‐Caete Guillermo Alcaín‐Martínez Natalia Ruiz‐Santana Luis Vzquez‐Pedreo Eduardo García‐Fuentes 《Obesity (Silver Spring, Md.)》2020,28(9):1708-1717
109.
110.
Jae Min Cho SeulKi Park Rajeshwary Ghosh Kellsey Ly Caroline Ramous Lauren Thompson Michele Hansen Maria Sara de Lima Coutinho Mattera Karla Maria Pires Maroua Ferhat Sohom Mookherjee Kevin J. Whitehead Kandis Carter Mrcio Buffolo Sihem Boudina J. David Symons 《Aging cell》2021,20(10)
Protein quality control mechanisms decline during the process of cardiac aging. This enables the accumulation of protein aggregates and damaged organelles that contribute to age‐associated cardiac dysfunction. Macroautophagy is the process by which post‐mitotic cells such as cardiomyocytes clear defective proteins and organelles. We hypothesized that late‐in‐life exercise training improves autophagy, protein aggregate clearance, and function that is otherwise dysregulated in hearts from old vs. adult mice. As expected, 24‐month‐old male C57BL/6J mice (old) exhibited repressed autophagosome formation and protein aggregate accumulation in the heart, systolic and diastolic dysfunction, and reduced exercise capacity vs. 8‐month‐old (adult) mice (all p < 0.05). To investigate the influence of late‐in‐life exercise training, additional cohorts of 21‐month‐old mice did (old‐ETR) or did not (old‐SED) complete a 3‐month progressive resistance treadmill running program. Body composition, exercise capacity, and soleus muscle citrate synthase activity improved in old‐ETR vs. old‐SED mice at 24 months (all p < 0.05). Importantly, protein expression of autophagy markers indicate trafficking of the autophagosome to the lysosome increased, protein aggregate clearance improved, and overall function was enhanced (all p < 0.05) in hearts from old‐ETR vs. old‐SED mice. These data provide the first evidence that a physiological intervention initiated late‐in‐life improves autophagic flux, protein aggregate clearance, and contractile performance in mouse hearts. 相似文献