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UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
polyclonal
Application:
immunofluorescence
immunohistochemistry
western blot
immunohistochemistry
western blot
Species reactivity:
rat, human
Citations:
1
Technique(s):
immunofluorescence: suitable
immunohistochemistry: suitable
western blot: suitable
immunohistochemistry: suitable
western blot: suitable
Uniprot accession no.:
产品名称
Anti-AMBRA1 Antibody, from rabbit, purified by affinity chromatography
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
rat, human
technique(s)
immunofluorescence: suitable
immunohistochemistry: suitable
western blot: suitable
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Quality Level
Gene Information
human ... AMBRA1(55626)
Analysis Note
Evaluated by Western Blotting in rat brain tissue lysate.
Western Blotting Analysis: 2 μg/mL of this antibody detected AMBRA1 in rat brain tissue lysate.
Western Blotting Analysis: 2 μg/mL of this antibody detected AMBRA1 in rat brain tissue lysate.
Application
Anti-AMBRA1 Antibody is an antibody against AMBRA1 for use in western blotting, IHC & immunofluorescence.
Immunohistochemistry Analysis: 5 μg/mL from a representative lot detected AMBRA1 in human brain tissue.
Immunofluorescence Analysis: 20 μg/mL from a representative lot detected AMBRA1 in human brain cells.
Immunofluorescence Analysis: 20 μg/mL from a representative lot detected AMBRA1 in human brain cells.
Research Category
Apoptosis & Cancer
Apoptosis & Cancer
Research Sub Category
Apoptosis - Additional
Apoptosis - Additional
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
General description
Autophagy, the process of bulk degradation of cellular proteins through an autophagosomic-lysosomal pathway is important for normal growth control and may be defective in tumor cells. It is involved in the preservation of cellular nutrients under starvation conditions as well as the normal turnover of cytosolic components. Beclin-1, a principal regulator of autophagosome formation (3), is in turn regulated by AMBRA1. AMBRA1 associates with Beclin-1 through a region near its center as determined by yeast two-hybrid assay. Null mutations in this gene in mice resulted in embryonic lethality with severe neural tube defects associated with autophagy impairment, accumulation of ubiquitinated proteins, unbalanced cell proliferation and excessive apoptotic death. Furthermore, down-regulation of AMBRA1 in cultured cells though RNA interference decreased the level of rapamycin and nutrient starvation-induced autophagy (4). Multiple isoforms of AMBRA1 are known to exist.
~150 kDa observed. Uncharacterized bands may be observed in some lysate(s). Uniprot describes 6 isoforms produced by alternative splicing ranging between ~84 kDa and ~143 kDa
Immunogen
Epitope: N-terminus
KLH-conjugated synthetic peptide corresponding to the N-terminus of human AMBRA1.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Physical form
Antigen Affinity Purified
Purified rabbit polyclonal in buffer containing PBS with up to 0.1% sodium azide.
Preparation Note
Stable for 1 year at 2-8°C from date of receipt.
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存储类别
12 - Non Combustible Liquids
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
Daniela Strobbe et al.
British journal of pharmacology, 178(2), 298-311 (2020-10-11)
The mitochondrial F1 Fo -ATPsynthase is pivotal for cellular homeostasis. When respiration is perturbed, its mode of action everts becoming an F1 Fo -ATPase and therefore consuming rather producing ATP. Such a reversion is an obvious target for pharmacological intervention
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