key: cord-0037626-pwmgngwn
authors: nan
title: Caspase-7
date: 2009-10-01
journal: Class 3 Hydrolases
DOI: 10.1007/978-3-540-85705-1_14
sha: f363f3f77d75446703c4949aedd52c55c13b5340
doc_id: 37626
cord_uid: pwmgngwn

nan

Natural substrates and products S epidermal growth factor receptor + H 2 O <2> (<2> cleavage during apoptosis [12] ) (Reversibility: ?) [12] P ? S kinectin + H 2 O <2> (<2> kinectin is cleaved by caspase 7 during apoptosis induced by different stimuli. Kinectin functions as a membrane anchor for kinesin and may be relevant to the disruption of vesicle trafficking during apoptosis [18] ) (Reversibility: ?) [18] P ? S poly(ADP-ribose) polymerase + H 2 O <2, 5> (<2> whereas caspase-7 can cleave poly(ADP-ribose) polymerase in vivo, a collaborating caspase facilitates access to poly(ADP-ribose) polymerase, possibly by enhancing nuclear entry [23] ; <5> the cleavage of poly(ADP-ribose) polymerase observed during apoptosis cannot solely be attributed to CPP32 but can als be an activity of Mch2a [15] ) (Reversibility: ?) [11, 15, 23 ] P ? S pro-endothelial monocyte-activating polypeptide II + H 2 O <1> (<1> caspase-7-mediated generation and release of mature endothelial monocyteactivating polypeptide II may provide a mechanism for leukocyte recruitment to sites of programmed cell death, and thus may link apoptosis to inflammation [22] ) (Reversibility: ?) [22] P ? S viral nucleocapsid protein of transmissible gastroenteritis coronovirus + H 2 O <2> (<2> cleavage site VVPD359-/-. Destruction of viral protein by the host cell death machinery [9] ) (Reversibility: ?) [9] P ? S Additional information <2, 6> (<6> overexpression induces apoptosis [8] ;

<2> caspase-7 is the most downstream caspase, overexpression does not lead to the activation of other caspases [23] ; <2> the enzyme is activated during Fas-and tumor necrosis factor-induced apoptosis [23, 24] [9] ; <2> cleavage site VVPD359-/-. Destruction of viral protein by the host cell death machinery [9] ) (Reversibility: ?) [9] P ? S Additional information <2, 5, 6> (<2> the preferred cleavage sequence is DEVD-/- [5, 6] ; <5> no cleavage of YVAD-7-amido-4-methylcoumarin [15] ; <5> no cleavage of interleukin 1b precursor [14] ; <6> overexpression induces apoptosis [8] ; <2> caspase-7 is the most downstream caspase, overexpression does not lead to the activation of other caspases [23] ; <2> the enzyme is activated during Fas-and tumor necrosis factorinduced apoptosis [23, 24] ) (Reversibility: ?) [5, 6, 8, 14, 15, 23, 24 ] P ?

AC-DEVD-aldehyde inhibitor <2> [34] AC-DQTD-CHO <2> [27] Ac-DEVD-CHO <2, 4> [27, 29] Ac-Z-Val-Ala-Asp-fluoromethylketone <2> [27] DEVD-CHO <2> [25] DEVD-aldehyde <5> (<5> potent inhibitor [15] ) [15] DEVD-fluoromethylketone <2> (<2> more specific than YVAD-cmk [12] ) [12] X-linked inhibitor of apoptosis <2> [30] YVAD-aldehyde <5> (<5> weak inhibitor [15] ) [15] YVAD-chloromethylketone <2> [12] Z-Val-Ala-Asp-fluoromethylketone <2, 3> (<2> inhibits Enterovirus 70-induced apoptosis and virus release, but not intracellular viral production [35] ) [26, 29, 30, 35] acetyl-AEVD-aldehyde <2> [3] acetyl-Ala-Pro-Nle-Asp-aldehyde <2> [13] acetyl-DEVD-aldehyde <2> [3, 11] acetyl-IETD-aldehyde <2> [3] benzyloxycarbonyl-ASTD-fluoromethylketone <1> (<1> 0.01 mM, complete inhibition of cleavage of pro-endothelial monocyte-activating polypeptide II [22] ) [22] benzyloxycarbonyl-DEVD-chloromethylketone <1> (<1> 0.01 mM, complete inhibition [22] ) [22] benzyloxycarbonyl-Pro-Nle-Asp-aldehyde <2> [13] benzyloxycarbonyl-VAD-[(2,6-dichlorobenzoyl)-oxy]methyl ketone <2> [11] benzyloxycarbonyl-VAD-fluoromethylketone <2> (<2> t 1=2 at 0.001 mM is 98 s [3] ) [3] cowpox seroin CrmA <5> (<5> very weak inhibitor [15] ) [15] ketonic peptides <2> (<2> in the straight-chain aliphatic series, increasing inhibition with increasing chain length, for the unsubstituted aromatic P1 inhibitors increasing potency with decreasing linker length [34] ) [34] Additional information <2> (<2> K i -values higher than 0.01 mM are determined for acetyl-WEHD-aldehyde and acetyl-YVAD-aldehyde and cowpox serin CrmA [3] ) [3] Activating compounds ceramide <2> [33] FSH <3> (<3> antiapoptotic effect on granulosa cells and a proapoptotic effect on theca-interstitial cells [26] ) [26] LH <3> (<3> antiapoptotic effect on granulosa cells and a proapoptotic effect on theca-interstitial cells [26] ) [26] apoptosome complex <2> [30] cytolethal distending toxin <2> (<2> from Actinobacillus actinomycetemcomitans [27] ) [27] gonadotropins <3> (<3> increases caspase-7 activity in both theca-interstitial cells and granulosa cells [26] ) [26] hypoxia <2> [33] nitric oxide <2> [33] topoisomerase II inhibitor etoposide <2> (<2> procaspase-7 cleavage (= activation of caspase-7), which is abrogated in cells with ectopically expressed p53 [25] ) [25] topoisomerase II poison etopside <2> [29] Additional information <3> (<3> caspase-7 activity not increased by IGF-I [26] ) [26] Turnover number (min -1 ) 1.26 <2> (Ac-VDVAD-p-nitroanilide) [ Subunits tetramer <2> [30] Additional information <2, 5> (<2> 2 * 35000, procaspase-7 C285A mutant, in the homodimeric procaspase-7 each monomer is organized in two structured subdomains connected by partially flexible linkers, which asymmetrically occupy and block the central cavity, SDS-PAGE [20] ; <5> it is proposed that the 22000 Da peptide and the 12000 Da peptide are two subunits of the enzyme [14, 15] ) [14, 15, 20] Posttranslational modification proteolytic modification <2, 5, 7> (<2> viral nucleocapsid protein of transmissible gastroenteritis coronavirus triggers the processing of procaspase 6 in human rectal tumor cell line HRT18jap1 [9] ; <5> Mch3a is made of two subunits derived from a precursor ProMch3a. Asp23 and Asp198 are the most likely processing sites. Bacterially expressed Mch3 has intrinsic autocatalytic and autoactivation activity [15] ; <7> enzyme is synthesized as an inactive 30000-35000 Da precursor and is thought to be cleaved during apopto-sis to generate active fragments of 20000 Da and 10000 Da [17] ; <2> the Npeptide of caspase-7 must be removed, probably be caspase-3, before efficient activation of the zymogen can occur in vivo. The N-peptide serves to physically sequester the caspase-7 zymogen in a cytosolic location that prevents access by upstream activators, caspase-8, caspase-9 and caspase-10 [23] ; <5> both Mch4 and the serine protease granzyme B cleave proMch3 at a conserved IXXD-S sequence to produce the large and small subunits of the active protease. Mch3 is a target of mature protease in apoptotic cells [7] ; <2> activation site is IQAD (P4,P3,P2,P1) [6] ; <2> the 12000 Da and the 11000 Da polypeptides are generated by processing of the CMH-1 protein at Asp198-Ser199 and to a lesser extent at Asp206-Ala207 [23] ; <5> CPP32 can efficiently cleave proMch3a [15] ) [6, 7, 9, 14, 15, 17, 23] 5 Isolation/Preparation/Mutation/Application Source/tissue Chang cell <2> (<2> conjunctival cell [35] ) [35] HEK-293 cell <2> [33] HRT-18 cell <2> [9] HeLa cell <2> [18, 28, 29] JURKAT cell <2> [18, 19, 24, 27, 29] MCF-7 cell <2> [30] MOLT-4 cell <2> [27] NCI-H1299 cell <2> [25] SH-SY5Y cell <2> [33] T-cell <5> [15] T-lymphocyte <2> [27] brain <1, 6> (<6> low activity [8] ) [8, 32] egg <4> [29] granulosa cell <3> [26] heart <6> [8] kidney <1, 6> [8, 32] liver <1, 6, 7> [8, 17, 32] lung <5, 6> (<5> fetal lung [16] ) [8, 16] neuron <2> [33] skeletal muscle <6> [8, 16] skin <5> [1] spleen <1, 5, 6> (<5> getal spleen [16] ) [8, 14, 16, 32] stomach <1> [32] tadpole <4> (<4> stage 62 tadpole tail [2] ) [2] tail <4> (<4> stage 62 tadpole tail [2] ) [2] telencephalon <1> (<1> precursor neurons [32] ) [32] testis <6> [8] Additional information <2, 3> (<2> NCI-H358 cell [25] ; <3> theca-interstitial cells, preovulatory follicles [26] ; <2> U3A cell, 2fTGH cell, G8 cell, 1CC cell, 1C5 cell [28] ) [25, 26, 28] Localization cytoplasm <2> [33] cytosol <1, 2, 7> [17, 18, 29, 32] nucleus <2, 4> (<4> caspase-7 is activated and accumulates in the nucleus. A prodomain of caspase-7, 31 amino acid residues, inhibits both the apoptosisinducing activity and the nuclear localization, removal of the prodomain induces both the nuclear import of the catalytic protease and the cell killing activity [21] ) [21, 29, 33] plasma membrane <7> (<7> juxtamembrane structures [17] ) [17] Additional information <2> (<2> human caspase-7 is not a nuclear caspase removal of the N-peptide does not allow an active transport or accumulation of human caspase-7 in the nuclei [23] ) [23] Purification <1> [32] <2> [32, 34] <2> (by nickel affinity chromatography, anion exchange chromatography and gel filtration) [31] <2> (partially purified X-linked inhibitor of apoptosis-caspase-7 complex by gel filtration and immunopurification, SDS-PAGE) [30] <5> [14] <7> [17] Crystallization <2> (2.9 A crystal structure of recombinant C285A procaspase, sitting drop vapor diffusion method) [20] Cloning <1> (cloned into the NcoI site of the pET11d vector and expression in Escherichia coli BL21codon+) [32] <2> [3, 24, 25, 31, 32] <2> (expression in CG1945 yeast strain) [33] <2> (expression in Escherichia coli) [34] <2> (expression in Escherichia coli BL21 (DE3) transformed with a pET-21b plasmid expression vector) [30] <4> [2] <5> (bacterially expressed Mch3 has intrinsic autocatalytic and autoactivation activity) [15] <5> (overexpression in COS cells) [14] <6> [8] <7> [17] Engineering C285A <2> (<2> mutant procaspase-7 shows no autoactivation [20] ) [20] Application medicine <1, 2, 4> (<2> Actinobacillus actinomycetemcomitans cytolethal distending toxin acts as an immunosuppressive factor, it possesses the ability to induce human T-cell apoptosis through activation of caspase-7 [27] ; <2> acute hemorrhagic conjunctivitis, Enterovirus 70 infection induces caspase-7-mediated apoptosis [35] ; <2,4> cleavage of claspin by caspase-7 inactivates the Chk1 signaling pathway, this mechanism may regulate the balance between cell cycle arrest and induction of apoptosis during response of genotoxic stress [29] ; <2> hydrophobic P5 residue has a favorable contribution to the recognition and hydrolysis of substrates but not by caspase-7, this information helps to design specific inhibitors for each caspase [31] ; <2> low-dosage topoisomerase II inhibitor etoposide effectively inhibits proliferation rate [25] ; <2> strong correlation between caspase-7 activity, normal brain development, and apoptotic DNA fragmenation in Casp3-/-mice [32] ; <1> strong correlation between caspase-7 activity, normal brain development, and apoptotic DNA fragmenation in Casp3-/-mice, caspase-7 is a caspase-3 surrogate in Casp3-/-mice [32] ; <2> substitution in the P1 position could be used in synergy with other elements to obtain highly potent and isozymeselective caspase inhibitors [34] ; <2> SUMO-1 modification in caspase-7 may contribute to the cleavage of nuclear substrates during neuronal apoptosis [33] ) [25, 27, 29, 31, 32, 33, 34, 35] Additional information <2> (<2> apoptosis is preceded by proteolytic cleavage of e.g. caspase 7, prolonged nuclear localization of activated signal transducer and activator of transcription 1 results in apoptosis involving specific regulation of caspase pathway [28] ) [28] 

<2> (acetyl-YQVD-4-nitroanilide

<2> (acetyl-VDQQD-4-nitroanilide

<2> (<2> reaction with acetyl-DEVD-7-amido-4-methylcoumarin [4]) [4] pH-Range 6-7 <7> (<7> pH 6.0: about 35% of maximal activity

Enzyme Structure Molecular weight 26000 <2> (<2> active form of caspase-7, Western blot analysis

<2> (<2> X-linked inhibitor of apoptosis-caspase-7 complex

Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences

Structure, expression, and function of the Xenopus laevis caspase family

Inhibition of human caspases by peptide-based and macromolecular inhibitors

Purification and catalytic properties of human caspase family members

Proteases from cell suicide: functions and regulation of caspases. Microbiol

A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis

In vitro activation of CPP32 and Mch3 by Mch4, a novel human apoptotic cysteine protease containing two FADD-like domains

Characterization of seven murine caspase family members

The viral nucleocapsid protein of transmissible gastroenteritis coronavirus (TGEV) is cleaved by caspase-6 and -7 during TGEV-induced apoptosis

Substrate specificities of caspase family proteases

Substrate and inhibitor specificity of interleukin-1b-converting enzyme and related caspases

Proteolytic cleavage of epidermal growth factor receptor by caspases

The caspase-like sites of proteasomes, their substrate specificity, new inhibitors and substrates, and allosteric interactions with the trypsin-like sites

Identification and characterization of CPP32/Mch2 homolog 1, a novel cysteine protease similar to CPP32

Mch3, a novel human apoptotic cysteine protease highly related to CPP32

Identification and mapping of Casp7, a cysteine protease resembling CPP32 b, interleukin-1 b converting enzyme, and CED-3

Purification and cDNA cloning of a second apoptosis-related cysteine protease that cleaves and activates sterol regulatory element binding proteins

Caspase 7-induced cleavage of kinectin in apoptotic cells

Caspase 7 can cleave tumor necrosis factor receptor-I (p60) at a non-consensus motif, in vitro

Structural basis for the activation of human procaspase-7

Inhibition of nuclear transport of caspase-7 by its prodomain

The endothelial monocyte-activating polypeptide II (EMAP II) is a substrate for caspase-7

Human caspase-7 activity and regulation by its N-terminal peptide

ICE-LAP-3, a novel mammalian homologue at the Caenorhabditis elegans cell death protein Ced-3 is activated during Fas-and tumor necrosis factor-induced apoptosis

Etoposide (VP-16) sensitizes p53-deficient human non-small cell lung cancer cells to caspase-7-mediated apoptosis

Gonadotropins enhance caspase-3 and -7 activity and apoptosis in the theca-interstitial cells of rat preovulatory follicles in culture

Caspase-2 and caspase-7 are involved in cytolethal distending toxin-induced apoptosis in Jurkat and MOLT-4 T-cell lines

STAT1-induced apoptosis is mediated by caspases 2, 3, and 7

Cleavage of claspin by caspase-7 during apoptosis inhibits the Chk1 pathway

Caspase-7 is directly activated by the approximately 700-kDa apoptosome complex and is released as a stable XIAP-caspase-7 approximately 200-kDa complex

Structural and kinetic analysis of caspase-3 reveals role for S5 binding site in substrate recognition

Caspase-7 expanded function and intrinsic expression level underlies strain-specific brain phenotype of caspase-3-null mice

Relationship between SUMO-1 modification of caspase-7 and its nuclear localization in human neuronal cells

Using peptidic inhibitors to systematically probe the S 1 site of caspase-3 and caspase-7

Caspase-3 and -7 mediate apoptosis of human Chang's conjunctival cells induced by enterovirus 70