3.4.22.62: caspase-9
This is an abbreviated version!
For detailed information about caspase-9, go to the full flat file.
Word Map on EC 3.4.22.62
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3.4.22.62
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caspase-3
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bcl-2
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parp
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anti-apoptotic
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pro-apoptotic
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tunel
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necrosis
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apoptosis-related
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caspase-dependent
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apoptosis-inducing
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jnk
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apaf-1
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annexin
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extrinsic
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cyclin
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leukemia
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bid
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neuroprotective
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depolarization
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polyadp-ribose
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survivin
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hoechst
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z-vad-fmk
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antiproliferative
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adp-ribose
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xiap
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iodide
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deoxynucleotidyl
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mitochondria-dependent
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mitochondria-mediated
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cisplatin
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dutp
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fadd
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procaspase-3
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caspase-mediated
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pan-caspase
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fas-mediated
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trail
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fas-associated
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trail-induced
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bcl-2-associated
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apoptogenic
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pharmacology
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cdc25c
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puma
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transferase-mediated
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executioner
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factor-related
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deltapsim
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medicine
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tunel-positive
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sub-g1
- 3.4.22.62
- caspase-3
- bcl-2
- parp
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anti-apoptotic
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pro-apoptotic
-
tunel
- necrosis
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apoptosis-related
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caspase-dependent
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apoptosis-inducing
- jnk
- apaf-1
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annexin
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extrinsic
- cyclin
- leukemia
- bid
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neuroprotective
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depolarization
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polyadp-ribose
- survivin
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hoechst
- z-vad-fmk
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antiproliferative
- adp-ribose
- xiap
- iodide
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deoxynucleotidyl
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mitochondria-dependent
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mitochondria-mediated
- cisplatin
- dutp
- fadd
- procaspase-3
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caspase-mediated
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pan-caspase
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fas-mediated
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trail
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fas-associated
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trail-induced
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bcl-2-associated
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apoptogenic
- pharmacology
- cdc25c
- puma
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transferase-mediated
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executioner
-
factor-related
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deltapsim
- medicine
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tunel-positive
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sub-g1
Reaction
strict requirement for an Asp residue at position P1 and with a marked preference for His at position P2. It has a preferred cleavage sequence of Leu-Gly-His-Asp-/-Xaa =
Synonyms
APAF, Apaf-3, apoptotic protease activating factor 3, apoptotic protease Mch-6, C14.010, CASP-9, casp9, casp9-gamma, caspase 9, caspase-9, ICE-LAP6, ICE-like apoptotic protease 6, Mch6
ECTree
3.4.22.62 caspase-9Advanced search results
results (
results (Inhibitors
Inhibitors on EC 3.4.22.62 - caspase-9
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INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
(3S,6S,10aS)-6-(L-alanylamino)-N-(diphenylmethyl)-5-oxodecahydropyrrolo[1,2-a]azocine-3-carboxamide
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(3S,6S,8aS)-6-(L-alanylamino)-N-(diphenylmethyl)-5-oxooctahydroindolizine-3-carboxamide
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(3S,6S,9aS)-6-(L-alanylamino)-N-(diphenylmethyl)-5-oxooctahydro-1H-pyrrolo[1,2-a]azepine-3-carboxamide
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acetyl-DVAD fluoromethyl ketone
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prediction of the tertiary structure of a caspase-9/inhibitor complex
ATP
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enzyme activity is inhibited in both normoxic and hypoxic groups. The IC50 increases 5fold following hypoxia, suggesting a hypoxia-induced modification of the ATP binding site. 70% inhibition by 1 mM
biotin-Val-Ala-Asp-fluoromethyl ketone
i.e. biotin-VAD-fmk, presence or absence of 50 microM inhibitor, caspase-9 activation analyzed by affinity labelling and immunoblotting
cadmium
anti-apoptotic cell survival function of cadmium, cadmium inhibits apoptosis induced by benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE) at non-cytotoxic concentrations, 40% and 52% inhibition at 10 and 20 microM cadmium chloride, respectively
caspase-9S
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transfection of renal epithelial cells with the dominant-negative inhibitor caspase-9S
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cytochrome c
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enzyme activity is inhibited in both normoxic and hypoxic groups. The IC50 increases 1.5fold following hypoxia, suggesting a hypoxia-induced modification of the cytochrome binding site. 70% inhibition by 0.003 mM
N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-N-[2-(2-fluorophenyl)ethyl]-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 51% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-N-[2-(2-methoxyphenyl)ethyl]-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 1% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-N-[2-(4-fluorophenyl)ethyl]-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72, 34% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-N-(2-cyclopropylethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 16% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-N-butyl-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h for caspase activity assay, 45% inhibition of caspase-3 activity in SAOS-2 cells
N-(2-amino-2-oxoethyl)-N-[2-(4-chlorophenyl)ethyl]-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 2% inhibition of caspase-3 activity in SAOS-2 cells
N-benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone
i.e. Z-VAD-FMK, treatment with 100 microM caspase inhibitor in combination with 100 microM cordycepin for 24 h suppresses sub-G1 phase in MA-10 cells
N-[2-(acetylamino)ethyl]-N-(2-amino-2-oxoethyl)-1-[2-(2,4-dichlorophenyl)ethyl]-4-(3,3-diphenylpropyl)-3,7-dioxo-1,4-diazepane-5-carboxamide
5 microM for cell treatment, cells harvested after 24, 48, and 72 h, 22% inhibition of caspase-3 activity in SAOS-2 cells
Pen-1-XBIR3
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caspase-9 is inhibited by unilateral intravitreal injection of highly specific X-linked inhibitor of apoptosis (IAP) baculoviral IAP repeat 3 (XBIR3) domain linked to the cell transduction peptide penetratin 1 (Pen-1) after ballistic injury
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Q-VD-OPH
i.e. (3S)-5-(2,6-difluorophenoxy)-3-[[(2S)-2-(isoquinoline-3-carbonylamino)-3-methylbutanoyl]amino]-4-oxopentanoic acid, cell treatment with the broad-spectrum caspase inhibitor Q-VD-OPH (concentration 30 microM) prior to induction of differentiation
RQIKIWFQNRRMKWKKGG-N-[2-(2,4-dichlorophenyl)ethyl]glycyl-N-(3,3-diphenylpropyl)glycyl-N2-[2-(2,4-dichlorophenyl)ethyl]glycinamide
i.e. PEN-1, modified compound with peptide bridge, 5 microM for cell treatment, shows low inhibitory activity of caspase-3
XIAP
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can antagonise caspase-9 activity and stabilises its interaction with the apoptosome. Caspase-3 cleaves XIAP into fragments that retain their inhibitory potential towards caspases-3 or -9, thereby eliminating sterical hindrance that may prevent parallel inhibition of caspases-3 and -9 by XIAP
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XIAP-BIR3
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a natural caspase-9 inhibitor that binds at the dimer interface keeping the enzyme in an inactive monomeric state, binding to the enzyme involves the alpha5 helix of XIAP-BIR3
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Z-IETD-fluoromethylketone
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a caspase-8 specific inhibitor, delays the activation of caspase-3 and caspase-9 significantly
Zn2+
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mixed-tpe inhibition, kinetics and mechanism of zinc-mediated inhibition of caspase-9, overview. Two distinct zinc-binding sites on caspase-9, the first site, composed of H237, C239, and C287, includes the active site dyad and is primarily responsible for zinc-mediated inhibition. The second binding site at C272 is distal from the active site. EDTA can hinder enzyme inhibition by Zn2+. Zinc-mediated inhibition does not influence the overall structure of caspase-9 monomers. Each wild-type caspase-9 monomer binds two zinc ions. Caspase-9 variants in which the active-site residues are replaced, C287A or H237A, bind just one zinc
benzyloxycarbonyl-LEHD-fluoromethylketone
cell transfection with siRNA against the cellular-FLICE inhibitory protein (c-FLIP) followed by the addition of the caspase-9 inhibitor benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone protects the cells from spontaneous apoptosis, indicates that c-FLIP siRNA-triggered apoptosis occurrs by a caspase-9-dependent process, inhibitor concentration of 20 microM for 48 h, apoptosis determined by counting fragmented nuclei using fluorescent dyes, caspase-9 activation shown by Western blot
benzyloxycarbonyl-LEHD-fluoromethylketone
i.e. z-LEHD-FMK, inhibitor effect on apoptosis induced by high linear energy transfer (LET) radiation, induction of apoptosis investigated at 48 h after 10 day irradiation in the presence of 2-100 microM inhibitor concentration, caspase-9 inhibitor suppresses caspase-3 activation and apoptosis induction by radiation to a greater extent than caspase-8 inhibitor
benzyloxycarbonyl-LEHD-fluoromethylketone
i.e. z-LEHD-FMK, specific caspase-9 inhibitor, concentration of 50 microM, inhibitor effect on isorhamnetin-induced apoptosis, cells exposed to DMSO or 40 microM isorhamnetin for 48 h
benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethylketone
i.e. z-LEHD-FMK, inhibitor concentration 100 microM
benzyloxycarbonyl-VAD-fluoromethylketone
i.e. Z-VAD-FMK, in vitro oocyte meiosis and fragmentation analyzed by treatment with concentrations of 50 and 100 microM, transition from metaphase I to metaphase II accelerated in oocytes, comparative treatment with the apoptotic inducer doxorubicin (DXR)
PGA-1
PGA-peptoid conjugate, inhibitor of apoptotic protease activating factor 1 (Apaf-1) coupled to poly-L-glutamic acid (PGA), at concentrations of 50 and 100 microM inhibition of caspase-3 activity, reaches values up to 100% at 50 microM drug after 48 h in HeLa-cells and and after 72 h in SAOS-2 cells
PGA-1
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PGA-peptoid 1, inhibitor (peptoid 1) of apoptotic protease activating factor 1 (Apaf-1) coupled to poly-L-glutamic acid (PGA)
Z-LEHD-fluoromethylketone
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a caspase-9 specific inhibitor, inhibits caspase-9 activation completely
additional information
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inhibition of caspase-9 enhances the viability of the CHO cells in both batch and fed-batch suspension cultures
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additional information
rituximab-induced apoptosis involved in the activation of caspase-9 can be blocked by Bcl-xL overexpression
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additional information
DYRK1A-dependent phosphorylation of Thr125 blocked by the kinase inhibitor harmine
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additional information
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DYRK1A-dependent phosphorylation of Thr125 blocked by the kinase inhibitor harmine
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additional information
caspase-9/-3 activation in differentiated cells, inhibited by protein kinase C (PKC) and the mitogen activated protein kinase (MEK) signaling pathways
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additional information
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development, design and synthesis, of three types of stabilized peptides derived from the alpha5 helix of inhibitor XIAP-BIR3, using incorporation of amino-isobutyric acid, the avian pancreatic polypeptide-scaffold or aliphatic staples, overview. The stabilized peptides are helical in solution and achieve good inhibition, indicating that this allosteric site at the caspase-9 dimerization interface is regulatable with low-molecular weight synthetic ligands and is thus a druggable site. Other caspases, which are not regulated by dimerization, are not inactivated by these peptides
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additional information
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caspase-3 can bind to the nucleotide binding domain of Apaf-1 on the apoptosome backbone. Binding eliminates the close association of caspase-9 with the nucleotide binding domain of Apaf-1, resulting in its inactivation
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additional information
activation of caspase-9 by Cd2+ is inhibited by treatment with the herbal drug Hwanggunchungyitang (HGCYT) in a dose-dependent manner, pretreatement of cells with 0.01-1 mg/ml inhibitor for 1 h, treatment with 10 microM Cd2+ for 24 h
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additional information
the protein kinase DYRK1A is a negative regulator of the intrinsic apoptotic pathway in the developing retina by phosphorylating caspase-9 on the inhibitory threonine residue 125 to prevent activation
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additional information
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the protein kinase DYRK1A is a negative regulator of the intrinsic apoptotic pathway in the developing retina by phosphorylating caspase-9 on the inhibitory threonine residue 125 to prevent activation
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additional information
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atorvastatin-mediated apoptosis of hepatic stellate cells (HSCs) can be bocked by co-treatment with mevalonic acid and U0126, an activator of the extracellular signal-regulated protein kinase (ERK1/2)
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