X
Search Filters
Format Format
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
index medicus (26) 26
animals (20) 20
mice (18) 18
article (12) 12
apoptosis (10) 10
biochemistry & molecular biology (10) 10
cell biology (9) 9
crystallography, x-ray (9) 9
humans (9) 9
male (8) 8
mice, knockout (8) 8
proteins (8) 8
research (7) 7
小学生 (7) 7
语文学习 (7) 7
阅读知识 (7) 7
amino acid sequence (6) 6
analysis (6) 6
bcl-2-associated x protein - metabolism (6) 6
biophysics (6) 6
cells (6) 6
crystals (6) 6
female (6) 6
membrane proteins - metabolism (6) 6
multidisciplinary sciences (6) 6
protein binding (6) 6
apoptosis regulatory proteins - metabolism (5) 5
bacterial proteins - chemistry (5) 5
bcl-2 homologous antagonist-killer protein - metabolism (5) 5
bcl-2-like protein 11 (5) 5
bh3 domains (5) 5
bh3 interacting domain death agonist protein - metabolism (5) 5
binding sites (5) 5
cell-death (5) 5
membrane proteins - chemistry (5) 5
molecular sequence data (5) 5
physiological aspects (5) 5
proto-oncogene proteins - metabolism (5) 5
课外阅读 (5) 5
activation (4) 4
bcl-2 homologous antagonist-killer protein - genetics (4) 4
bh3-only proteins (4) 4
biochemical research methods (4) 4
biological phenomena, cell phenomena, and immunity (4) 4
c-di-gmp (4) 4
cells, cultured (4) 4
crystallization (4) 4
crystallography (4) 4
cytochrome-c (4) 4
expression (4) 4
genetic aspects (4) 4
membrane proteins - genetics (4) 4
mitochondria - metabolism (4) 4
mitochondrial apoptosis (4) 4
models, biological (4) 4
sequence alignment (4) 4
structure (4) 4
tumor suppressor proteins - metabolism (4) 4
xanthomonas campestris (4) 4
amp (3) 3
apoptosis regulatory proteins - genetics (3) 3
bacterial proteins - metabolism (3) 3
bax (3) 3
bcl-2 family-members (3) 3
bcl-2-associated x protein - chemistry (3) 3
bcl-2-associated x protein - genetics (3) 3
bh3 interacting domain death agonist protein - genetics (3) 3
binding (3) 3
biological response modifiers (3) 3
cell death (3) 3
cell line, tumor (3) 3
crystal-structure (3) 3
crystallization communications (3) 3
cyclic gmp - analogs & derivatives (3) 3
cyclic gmp - metabolism (3) 3
c‐di‐gmp (3) 3
developmental biology (3) 3
gene expression (3) 3
gene-expression (3) 3
genotype (3) 3
innate immune receptors (3) 3
membrane permeabilization (3) 3
models, molecular (3) 3
mouse sting (3) 3
mutation (3) 3
proapoptotic bax (3) 3
protein (3) 3
protein multimerization (3) 3
protein structure, tertiary (3) 3
proto-oncogene proteins - genetics (3) 3
proto-oncogene proteins c-bcl-2 - metabolism (3) 3
risk factors (3) 3
stem-cells (3) 3
structural basis (3) 3
tumor suppressor proteins - genetics (3) 3
tumors (3) 3
abridged index medicus (2) 2
adult (2) 2
aged (2) 2
aged, 80 and over (2) 2
more...
Library Location Library Location
Language Language
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Molecular Cell, ISSN 1097-2765, 11/2009, Volume 36, Issue 3, pp. 487 - 499
While activation of BAX/BAK by BH3-only molecules (BH3s) is essential for mitochondrial apoptosis, the underlying mechanisms remain unsettled. Here we... 
CELLCYCLE | CYTOCHROME-C | PROAPOPTOTIC BAX | OLIGOMERIZES BAK | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOPLASMIC-RETICULUM | SUBCELLULAR LOCATION | PROTEINS | BCL-2 FAMILY-MEMBERS | BH3 DOMAIN | CELL-DEATH | MEMBRANE PERMEABILIZATION | CELL BIOLOGY | bcl-2-Associated X Protein - chemistry | Immunoprecipitation | Apoptosis - drug effects | Protein Multimerization | bcl-2 Homologous Antagonist-Killer Protein - genetics | Immunoblotting | BH3 Interacting Domain Death Agonist Protein - genetics | Green Fluorescent Proteins - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Bcl-2-Like Protein 11 | Protein Binding - drug effects | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Fibroblasts - metabolism | Proto-Oncogene Proteins - metabolism | Green Fluorescent Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Etoposide - pharmacology | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Tunicamycin - pharmacology | Fibroblasts - drug effects | Thapsigargin - pharmacology | Fibroblasts - cytology | Mice | Mutation | Microscopy, Fluorescence | Staurosporine - pharmacology | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Monomers | Apoptosis | Oligomers
Journal Article
Journal Article
Science, ISSN 0036-8075, 12/2010, Volume 330, Issue 6009, pp. 1390 - 1393
Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in... 
T lymphocytes | Mitochondria | Cytokines | Thymocytes | Neurons | Cell death | REPORTS | Cytochromes | Mice | Potassium | Apoptosis | NEURONAL APOPTOSIS | CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | MECHANISM | MULTIDISCIPLINARY SCIENCES | BH3 DOMAINS | RELEASE | JNK PATHWAY | PROTEINS | BCL-2 FAMILY-MEMBERS | MEMBRANE PERMEABILIZATION | BH3 Interacting Domain Death Agonist Protein - deficiency | T-Lymphocytes - physiology | bcl-2-Associated X Protein - chemistry | Protein Multimerization | Stress, Physiological | bcl-2 Homologous Antagonist-Killer Protein - genetics | BH3 Interacting Domain Death Agonist Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Membrane Proteins - deficiency | Caspases - metabolism | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - deficiency | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Neurons - physiology | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Permeability | Proto-Oncogene Proteins - deficiency | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Cerebellum - cytology | Intracellular Membranes - metabolism | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Protein research | Genetic aspects | Mitochondrial DNA | Biochemical genetics | Research | Properties | Methods
Journal Article
Nature Cell Biology, ISSN 1465-7392, 10/2015, Volume 17, Issue 10, pp. 1270 - 1281
Multidomain pro-apoptotic BAX and BAK, once activated, permeabilize mitochondria to trigger apoptosis, whereas anti-apoptotic BCL-2 members preserve... 
CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | ACTIVATION | CONFORMATIONAL-CHANGE | MEMBERS | PROAPOPTOTIC BAX | BH3 DOMAINS | PUMA | BH3-ONLY PROTEINS | MEMBRANE PERMEABILIZATION | CELL BIOLOGY | bcl-2 Homologous Antagonist-Killer Protein - genetics | Immunoblotting | BH3 Interacting Domain Death Agonist Protein - genetics | Cytochromes c - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Embryo, Mammalian - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Bcl-2-Like Protein 11 | Mitochondria - genetics | RNA Interference | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Fibroblasts - metabolism | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Mice, Inbred C57BL | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Intestine, Small - cytology | Embryo, Mammalian - cytology | Models, Biological | Fibroblasts - cytology | Intestine, Small - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics | Apoptosis | Genotype | Genetic aspects | Properties | Cell death | Cellular control mechanisms
Journal Article
Journal Article
Journal of Structural Biology, ISSN 1047-8477, 09/2019, Volume 207, Issue 3, pp. 260 - 269
Journal Article
Developmental Cell, ISSN 1534-5807, 02/2018, Volume 44, Issue 4, pp. 447 - 459.e5
Most cells in the liver are polyploid, but the functional role of polyploidy is unknown. Polyploidization occurs through cytokinesis failure and... 
Anln | polyploidy | mouse model | cytokinesis | liver cancer | hepatocellular carcinoma | E2f8 | DNA-PLOIDY PATTERN | CELL-DIVISION | ANEUPLOIDY | HEPATOCELLULAR-CARCINOMA | CYTOKINESIS | HEPATOCYTES | CANCER GENOME | MICE | DEVELOPMENTAL BIOLOGY | MUTATIONS | MOUSE MODELS | CELL BIOLOGY | Physiological aspects | Liver cancer | Analysis | Risk factors
Journal Article
Gastroenterology, ISSN 0016-5085, 04/2018, Volume 154, Issue 5, pp. 1421 - 1434
Cytokinesis can fail during normal postnatal liver development, leading to polyploid hepatocytes. We investigated whether inhibiting cytokinesis in the liver... 
Hepatic Carcinogenesis | Tumorigenesis | RNA Interference | Cell Cycle | TRANSFORMATION | PROGNOSIS | FAILURE | CANCER | RHOA | CELL-DIVISION | ANEUPLOIDY | ANLN | HEPATOCELLULAR-CARCINOMA | GASTROENTEROLOGY & HEPATOLOGY | Carcinoma, Hepatocellular - prevention & control | Humans | Hepatocytes - pathology | Hepatocytes - metabolism | Hepatectomy | Transfection | Time Factors | Cell Transformation, Neoplastic - genetics | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Microfilament Proteins - metabolism | Chemical and Drug Induced Liver Injury - pathology | Hepatocytes - transplantation | Microfilament Proteins - genetics | Liver Neoplasms - prevention & control | Cell Line | Genetic Predisposition to Disease | Liver Regeneration | Microfilament Proteins - deficiency | Liver Neoplasms - genetics | Chemical and Drug Induced Liver Injury - genetics | Cytokinesis | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Mice, Knockout | Carrier Proteins - genetics | Phenotype | Animals | Chemical and Drug Induced Liver Injury - metabolism | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Proto-Oncogene Proteins c-myc - genetics | Cell Transformation, Neoplastic - pathology | Carcinoma, Hepatocellular - metabolism | Liver cancer | RNA | Actin | Analysis | Carbon tetrachloride | Muscle proteins | Gene expression | Protein binding | hepatic carcinogenesis | RNA interference | tumorigenesis | cell cycle
Journal Article
Developmental Cell, ISSN 1534-5807, 11/2018, Volume 47, Issue 3, pp. 390 - 390
Journal Article