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Autophagy Pathway

 Autophagy,the 2016 Nobel Prize in Physiology or Medicine, is a dynamic cellular recycling system that results in the autophagosomic-lysosomal degradation of bulk cytoplasmic contents, abnormal protein aggregates, and excess or damaged organelles. The critical regulator of autophagy induction is mTOR kinase, that activated mTOR (Akt and MAPK signaling) suppressing autophagy, and negative regulation of mTOR (AMPK and p53 signaling) promoting it. The ULK which play a similar role as the yeast Atg1, act downstream of the mTOR complex. ULK forms a large complex with Atg13 and the scaffold protein FIP200. Class III PI3K complex, containing hVps34, Beclin-1 (a mammalian homolog of yeast Atg6), p150 (a mammalian homolog of yeast Vps15), and Atg14-like protein (Atg14L or Barkor) or ultraviolet irradiation resistance-associated gene (UVRAG), is required for the induction of autophagy. Rubicon inhibits PI3K class III lipid kinase activity and opposes the action of Atg14L, an enhancer of PI3K class III activity. The Atg genes control the autophagosome formation through Atg12-Atg5 and LC3-II (Atg8-II) complexes. Atg12 is conjugated to Atg5 in a ubiquitin-like reaction that requires Atg7 and Atg10 (E1 and E2-like enzymes, respectively). The Atg12–Atg5 conjugate then interacts noncovalently with Atg16 to form a large complex. The second complex, LC3/Atg8, is cleaved at its C-terminus by Atg4 protease to generate the cytosolic LC3-I. LC3-I is conjugated to phosphatidylethanolamine (PE) in a ubiquitin-like reaction that requires Atg7 and Atg3 (E1 and E2-like enzymes, respectively). The lipidated form of LC3, known as LC3-II, is attached to the autophagosome membrane. Autophagy and apoptosis are connected both positively and negatively, and extensive crosstalk exists between the two processes. During nutrient deficiency, autophagy functions as a pro-survival mechanism; however, excessive autophagy may lead to cell death, a process morphologically distinct from apoptosis. Several pro-apoptotic signals, such as TNF, TRAIL, and FADD, also induce autophagy. Additionally, Bcl-2 inhibits Beclin-1-dependent autophagy, thereby functioning both as a pro-survival and as an anti-autophagic regulator.

Groth Factor Cytokines Receptor Integrins RTK's GPCR alpha-Adrenergic Receptor Insulin Receptor AKT Signaling pathway MAPK-Erk Pathway P53 Pathway AMPK Signaling pathway mTOR MLST9 Raptor PRAS40 ULK ULK FIP200 Atg13 Atg11 Vac8 FIP200 Atg13 Atg11 Vac8 Rubicon Ambra Beclin 1 P53 HMGB1 Bmf JNK Bcl2 Ambra Atg14 Beclin 1 UVRAG Atg9 Vps34 PIK3R Atg2 Atg9 Atg18 Atg16l Atg16l Atg12 Atg5 Atg5 Atg12 Atg10 Atg12 Atg7 LC3B Atg3 LC3A Atg4 LC3 LC3B Rab Autophagosome Lysome Lysome Autophagolysosome Preautophagosome

Actin Dynamics Signaling Pathway from A to Z

SINGLE COMPONENTS PRODUCTS
alpha-Adrenergic Receptor search result
Ambra search result
Atg10 search result
Atg11 search result
Atg12 search result
Atg13 search result
Atg14 search result
Atg16l search result
Atg18 search result
Atg2 search result
Atg3 search result
Atg4 search result
Atg5 search result
Atg7 search result
Atg9 search result
Autophagosome search result
Bcl2 search result
Beclin 1 search result
Bmf search result
Cytokines Receptor search result
FIP200 search result
GPCR search result
Groth Factor search result
HMGB1 search result
Insulin search result
Insulin Receptor search result
Integrins search result
JNK search result
LC3 search result
LC3A search result
LC3B search result
Lysome search result
MLST9 search result
mTOR search result
P53 search result
PIK3R search result
PRAS40 search result
Raptor search result
RTK's search result
Rubicon search result
ULK search result
UVRAG search result
Vac8 search result
AKT Signaling pathway search result
MAPK-Erk Pathway search result
P53 Pathway search result
AMPK Signaling pathway search result
Vps34 search result
Rab search result
Autophagolysosome search result
Preautophagosome search result

Thanks to Sino Biological for providing the pathways.