| 1. | |
BCL2 family proteins-BCL-2, BCL-XL | Anti-apoptotic proteins (BCL-2, BCL-XL) bind BH3-only ligands,thereby inhibiting BAX/BAK-mediated apoptosis [Emily HY et al. Mol Cell 8:705 (2001)]. |  |
| 2. | |
BCL2 family proteins: BCL-2, BCL-XL | Anti-apoptotic proteins (BCL-2, BCL-XL) bind BH3-only ligands,thereby inhibiting BAX/BAK-mediated apoptosis [Emily HY et al. Mol Cell 8:705 (2001)]. * 해당강의는 동영상 촬영 시부터 마이크의 호환 문제로 강의 뒷부분에 교수자 음성이 녹음 되지 못하였습니다. |
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| 3. | |
BCL2 family proteins-BH3 ligands | BH3-only proteins induce apoptosis by inhibitig the anti-apoptotic family proteins, not activating pro-apoptotic proteins [Willis SN et al. Science 315:856 (2007)]. | |
| 4. | |
Wnt-β-Catenin pathway-Wnt5a and cellular invasion | Overexpression of Wnt5a in melanoma cells results in enhancement of PKC activation, cell motility and invasion [Weeraratna AT et al. Cancer Cell 1:279 (2002)]. | |
| 5. | |
Wnt-β-Catenin pathway-Lgr5+ stem cells as the origin of intestinal cancer | Stem-cell specific loss of Apc (one of the key proteins in Wnt-β-Catenin pathway) leads to interstinal neoplasia [Baker N et al. Nature 457:608 (2009)]. | |
| 6. | |
JAK-STAT pathway: Jak2 V617F mutation in Polycythaemia vera | Jak2 V617F mutation is identified in patients with Polycythaemia vera. The mutation caused constitutive tyrosine kinase activity, cytokine hypersensitivity and erythrocytosis [James C et al. Nature 434:1144 (2005)]. | |
| 7. | |
JAK-STAT pathway: Jak2 exon 12 mutations in Polycythaemia vera and Idiopathic Erythrocytosis | Identification of Jak2 exon 12 mutations in V617F-negative patients with myeloproliferative disorders. The mutations including K539L show similar phenotypes dercribed in V617F mutantion [Scott LM et al. N Engl J Med 356:459 (2009)]. | |
| 8. | |
Ubiquitination: HDM2 ubiquitin ligase inhibitor | Small molecules (HLI98) are identified as inhibitors of HDM2 E3 ubiqutin ligase. These compounds stabilize and activate p53 in cells, which resulting in induction of p53-dependent apoptosis [Yang et al. Cancer Cell 7:547 (2004)]. | |
| 9. | |
Ubiquitination: caspase 8 ubiquitination and activation | Death receptor ligation induces cullin3-based polyubiquitination of caspase 8. This polyubiquitination leads to p62-dependent aggregation and activation of caspase 8 in extrinsic apoptosis pathway [Jin Z et al. Cell 137:721 (2009)]. | |
| 10. | |
Insulin: IRS-1 S307 phosphorylation, Insulin: a role of JNK1 in obesity and insulin resistance | Tumor necrosis factor a inhibits insulin action. TNFa promotes the activation of the Jun NH2-terminal kinase. The JNK associates with insulin receptor substrate-1 and phosphorylates at ser307, which leading to insulin resistance. [Aguirre V et al. J Biol Chem 275:9047 (2000)]. Obesity is closely associated with insulin resistance and establishes the leading risk factor for type 2 diabetes mellitus. JNK activity is abnormally elevated in obesity. Studies of JNK1-null mice show that JNK1 deficiency results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity [Hirosuml J et al. Nature 420:333 (2002)]. |
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| 11. | |
Markers in colorectal cancer: BRAF mutations, Markers in colorectal cancer: EGFR mutation in 3'-untranslated region | BRAF missense mutations were identified in human cancers. All mutations are within the kinase domain, with a single substitution (V599E) accounting for 80%. Mutated BRAF proteins have enhanced kinase activity and are transforming in NIH3T3 cells. The V599E mutation activates cell growth in Ras-independent manner by mimicking phosphorylation of T598 and S601 that occurs during normal signaling [Davles H et al. Nature 417:949 (2002)]. An A13 repeat within the 3'-untranslated region of epidermal growth factor receptor is frequently mutated in microsatellite instability colon cancers and is associated with increased EGFR expression [Yuan Z et al. Cancer Res 69:7811 (2009)]. |
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