8-Br-cADPR
8-Br-cADPR (8-Bromo-Cyclic ADP-Ribose), a cyclic adenosine diphosphate (ADP)-ribose (cADPR) antagonist, is a TRPM2 ion channel antagonist. 8-Br-cADPR reduces renal damage and the expression of caspase-3 and TRPM2.
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- CAS No.: 151898-26-9
- Formule: C15H20BrN5O13P2
- Masse moléculaire:620.20
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
Chemical Information
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CAS No. 151898-26-9
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Masse moléculaire 620.20
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Formule C15H20BrN5O13P2
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SMILES
O[C@H]1[C@@H](O)[C@H](N2C(Br)=NC3=C2N=CN([C@H]4[C@H](O)[C@H](O)[C@@H](COP(O5)(O)=O)O4)C3=N)O[C@@H]1COP5(O)=O
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Synonyms
8-Bromo-Cyclic ADP-Ribose
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Two-electrode voltage clamp in Xenopus oocytes
Two-electrode voltage clamp measures whole-oocyte membrane current from Xenopus oocytes expressing exogenous ion channels, receptors, or transporters; one intracellular microelectrode senses membrane voltage, and the second injects current so the amplifier can hold the membrane at command voltages while recording the compensating current as the functional readout. The method is suited to Xenopus oocytes because their large size supports microinjection and intracellular electrode impalement, but the large membrane area can limit voltage-clamp speed and accuracy, especially for large or fast currents.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)