Bad
BAD is a pro-apoptotic BH3-only Bcl-2 family protein that promotes apoptosis by binding Bcl-xL and Bcl-2, displacing BAX, and reversing death-repressor activity[1]. Mechanistically, survival-factor signaling phosphorylates BAD, causing 14-3-3 binding rather than Bcl-xL binding, while Akt phosphorylation blocks BAD-induced neuronal death[2][3]. Therefore, BAD links growth-factor survival pathways to the intrinsic mitochondrial apoptosis machinery, where Bcl-2 family interactions control apoptotic commitment[3][4]. In disease-relevant metabolic models, BAD resides in a glucokinase-containing mitochondrial complex that integrates glycolysis and apoptosis, and BAD deficiency or non-phosphorylatable BAD mutants impair glucose homeostasis[5]. In pancreatic β-cells, BAD supports glucose-stimulated insulin secretion and β-cell survival, giving BAD practical value in diabetes-related apoptosis and metabolism studies[6]. Compared with activator isoforms such as BID, BIM, and PUMA, BAD functions mainly as a sensitizer that neutralizes anti-apoptotic Bcl-2 proteins rather than directly activating BAX-BAK[4]. For experimental applications, phospho-BAD BH3 helix mimetics activate glucokinase through a mechanism distinct from classical allosteric activators[7].
Références:
- [1]. Yang E, et al. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell. 1995 Jan 27;80(2):285-91. [Content Brief]
- [2]. Zha J, et al. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L). Cell. 1996 Nov 15;87(4):619-28. [Content Brief]
- [3]. Datta SR, et al. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell. 1997 Oct 17;91(2):231-41. [Content Brief]
- [4]. Hongay CF, et al. Antisense transcription controls cell fate in Saccharomyces cerevisiae. Cell. 2006 Nov 17;127(4):735-45. [Content Brief]
- [5]. Danial NN, et al. BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis. Nature. 2003 Aug 21;424(6951):952-6. [Content Brief]
- [6]. Danial NN, et al. Dual role of proapoptotic BAD in insulin secretion and beta cell survival. Nat Med. 2008 Feb;14(2):144-53. [Content Brief]
- [7]. Szlyk B, et al. A phospho-BAD BH3 helix activates glucokinase by a mechanism distinct from that of allosteric activators. Nat Struct Mol Biol. 2014 Jan;21(1):36-42. [Content Brief]
All Product Categories
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Bad Produits associés (6)
Produits associés (6)
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ML281
0 ImagesML281 is a highly selective inhibitor of serine/threonine kinase 33 (STK33) with an IC50 value of 14 nM. ML281 shows 700-fold selectivity over PKA and 550-fold over AurB. ML281 exerts core mechanism by inhibiting STK33: in small cell lung cancer, ML281 downregulates RPS6/BAD signaling phosphorylation, induces apoptosis, and suppresses proliferation, invasion. ML281 reduces STK33-mediated 4-hydroxyphenylpyruvate dioxygenase (HPD) phosphorylation in tyrosinemia . ML281 is suitable for research on STK33 function, KRAS mutation-related cancers (pancreatic cancer, colon cancer, lung adenocarcinoma, etc.), small cell lung cancer, and tyrosinemia-related damage
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Caudatin
0 ImagesCaudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease.
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XAN-5
0 ImagesCat. No.: HY-181599XAN-5 is a mitochondrial DNA G-quadruplex (mtG4) ligand with a Kd of 3.8 μM. XAN-5 selectively binds and stabilizes mtG4 structures, disrupting mitochondrial gene transcription and DNA replication. XAN-5 triggers mitochondrial dysfunction, ROS overproduction, G0 phase arrest and caspase-dependent apoptosis. XAN-5 inhibits autophagy and induces immunogenic cell death. XAN-5 inhibits tumor growth in a mouse liver cancer model while enhancing tumor-infiltrating CD4+ and CD8+ T cells. XAN-5 targets two cancer resistance mechanisms simultaneously. XAN-5 can be used for the research of liver cancer.
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Tubulin polymerization-IN-85
0 ImagesCat. No.: HY-180190Tubulin polymerization-IN-85 (Compound C21) is a tubulin polymerization inhibitor (IC50 = 1.59 μM) targeting the colchicine binding site. Tubulin polymerization-IN-85 can cause cancer cells G2/M phase arrest and induce apoptosis. Tubulin polymerization-IN-85 downregulates the expression of Bcl-2, Bcl-xl, Mcl-1, Cyclin B1, cdc25, cdc2 protein and upregulates P53, P21, Bad and Bax levels. Tubulin polymerization-IN-85 can be used for the research of cancer, such as cervical cancer.
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FLC-8
0 ImagesCat. No.: HY-182937CAS No.: 3100242-36-9FLC-8 is an orally active FLT3 inhibitor with IC50 values of 10.2 nM, 11.6 nM and 24.10 nM against human FLT3-WT, FLT3-G697R and FLT3-N676D, respectively. FLC-8 inhibits FLT3 autophosphorylation and downstream STAT5, AKT and ERK signaling pathways, and induces apoptosis in acute myeloid leukemia (AML) cells. FLC-8 exhibits potent antitumor activity in the MV4-11 xenograft model. FLC-8 can be used for the research of acute myeloid leukemia.
