Autophagy分析套組
Biovision提供Autophagy inhibitor抑劑劑、inducers誘導劑、及相關抗體。
Autophagy works as a cellular
housekeeper by eliminating defective proteins and organelles, the prevention of
abnormal protein aggregate accumulation, and the removal of intracellular
pathogens. Such functions are likely critical for autophagy-mediated protection
against aging, cancer, neurodegenerative diseases, and infection. It is a bulk
degradation system that delivers cytoplasmic constituents into lysosomes and
the clearance of old/damaged organelles, long-lived proteins, insoluble protein
aggregates and lipid droplets. This enables the reuse of intracellular
constituents such as an amino acid pool during periods of starvation and
regulates cellular homeostasis, cell death/survival, and lipid metabolism.
Autophagy can be divided into three main forms: microautophagy,
chaperone-mediated autophagy and macroautophagy. In microautophagy and the
mammalian-specific chaperone-mediated autophagy the lysosome directly engulfs
small portions of cytosol or receives chaperone-associated cargoes, respectively.
Macroautophagy involves the autophagosome, a double-membrane-bound vesicle,
which fuses with a lysosome to form the autophagolysosome, which is responsible
for the turnover of organelles (e.g., mitochondria) and portions of cytosol.
Autophagosome formation is mediated by the coordinated action of
autophagy-related genes (Atg's). Studies in yeast have resulted in the
discovery of over 30 Atg's. More recent work has identified their mammalian
counterparts, such as ULK1 (Atg1), Atg3–5, beclin-1 (Atg6), Atg7, LC3 (Atg8),
Atg9a, Atg10, Atg12, Atg13L, Atg14L, Atg16L1, FIP200 (Atg17), and WIPI-1
(Atg18) and denote that Atg's are highly conserved between yeast and mammals.
Antigen presentation, innate immune signaling, and pathogen degradation may all
involve autophagosome recruitment and activity, which suggests autophagy, plays
an important role in immunity and defense against infectious diseases. However,
defects in the autophagic response has been linked to a significant number of
human pathological conditions, which in turn, have been linked to the mTOR,
PTEN/PI3-K, TLR pathways, and innate immune responses. Many neurodegenerative
conditions can be traced back to defects in the autophagic response. The role
of autophagy in Huntington's disease, Parkinson's disease, Amyotrophic lateral
sclerosis, or Alzheimer's disease may reside in the failure to clear aggregates
of mutated toxic proteins. Autophagy has also been identified as a crucial
process in oncogenesis and cancer progression. Several autophagy-related proteins
have tumor suppressor activities (Beclin-1, Atg5, Bif-1, Atg4C, and UVRAG).
Some mutations in the autophagy-related genes (detected in humans or induced in
cellular or animal models) appear to result in an accumulation of DNA damage
and genome instability. Several reports have suggested that later, as a tumor
grows, cancer cells may need autophagy to survive nutrient-limiting and
low-oxygen conditions, especially in the internal region of the tumor that is
poorly vascularized. Autophagy may also protect some cancer cells against
ionizing radiation, possibly by removing damaged macromolecules or organelles,
such as mitochondria, which could protect against apoptosis and allow continued
survival of transformed cells. BioVision offers wide range of autophagy
inducers and inhibitors as well as antibodies against autophagy related
proteins.
Autophagy Inducers
1828-100 | 100 mg | |
1828-500 | 500 mg | |
1686-5 | 5 mg | |
1827-10 | 10 mg | |
1856-5 | 5 mg | |
1856-25 | 25 mg |
Autophagy Inhibitors
1685-5 | ATM | 5 mg |
1829-50 | 50 µg | |
1829-250 | 250 µg | |
1825-100 | 100 mg | |
1825-500 | 500 mg | |
1785-500 | 500 µg | |
1711-500 | 500 µg | |
2037-5 | 5 mg | |
2037-25 | 25 mg |
Autophagy
3113-100 | 100 µg | |
3110-100 | 100 µg | |
3169-100 | 100 µg | |
3117-100 | 100 µg | |
3910-100 | 100 µg | |
3912-100 | 100 µg | |
3912BP-50 | 50 µg | |
3916-100 | 100 µg | |
3916BP-50 | 50 µg | |
3886BP-50 |
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