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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Caspase 2, apoptosis-related cysteine peptidase

caspase-2, Ich-1
This gene encodes a member of the cysteine-aspartic acid protease (caspase) family. Caspases mediate cellular apoptosis through the proteolytic cleavage of specific protein substrates. The encoded protein may function in stress-induced cell death pathways, cell cycle maintenance, and the suppression of tumorigenesis. Increased expression of this gene may play a role in neurodegenerative disorders including Alzheimer's disease, Huntington's disease and temporal lobe epilepsy. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Jan 2011] (from NCBI)
Top mentioned proteins: PrP, caspase-3, caspase-9, CAN, caspase-8
Papers using caspase-2 antibodies
Regulation of p53 stability and function in HCT116 colon cancer cells.
Zhou Zhongjun, In PLoS ONE, 2003
... inhibitor (Z-DEVD-FMK), caspase-8 inhibitor (Z-IETD-FMK), caspase-family inhibitor (Z-VAD-FMK), caspase-1 inhibitor (Z-YVAD-FMK), caspase-10 inhibitor (Z-AEVD-FMK) and caspase-2 inhibitor (Z-VDVAD-FMK) were purchased from BioVision.
Botulinum neurotoxin C initiates two different programs for neurite degeneration and neuronal apoptosis
Nicotera Pierluigi et al., In The Journal of Cell Biology, 2002
... The caspase-2 inhibitor z-VD(OMe)VAD (OMe)-fmk was purchased from MP Biomedicals.
Secondary necrosis is a source of proteolytically modified forms of specific intracellular autoantigens: implications for autoimmunity
Casiano Carlos A et al., In Molecular Cancer, 2000
... Staurosporine (STS), N-acetyl-Asp-Glu-Val-Asp-7-amino-4-methylcoumarin (Ac-DEVD-AMC, fluorogenic caspase-3/7 substrate), and Ac-VDVAD-AMC (fluorogenic caspase-2 substrate) were purchased from Axxora.
Caspase knockoutsmatters of life and death
Rosen Antony et al., In The Journal of Cell Biology, 1998
... Anti–caspase-2 antibody sc623 and its corresponding blocking peptide were purchased from Santa Cruz Biotechnology, Inc ...
Papers on caspase-2
Flubendazole induces mitotic catastrophe and senescence in colon cancer cells in vitro.
Skálová et al., Hradec Králové, Czech Republic. In J Pharm Pharmacol, Feb 2016
This was accompanied by decrease in cyclin D1 levels, increase in cyclin B1 levels, activation of caspase 2 and caspase 3/7 and PARP cleavage.
Characterization and expression analysis of a caspase-2 in an invertebrate echinoderm sea cumber Apostichopus japonicus.
Li et al., Dalian, China. In Fish Shellfish Immunol, Jan 2016
Caspase-2 is the most evolutionarily conserved member of the caspase family which mediates the programmed cell death and plays crucial roles in key cellular processes.
Glycogen Synthase Kinase-3β and Caspase-2 Mediate Ceramide- and Etoposide-Induced Apoptosis by Regulating the Lysosomal-Mitochondrial Axis.
Chen et al., Taipei, Taiwan. In Plos One, Dec 2015
Glycogen synthase kinase-3β (GSK-3β) regulates the sequential activation of caspase-2 and caspase-8 before mitochondrial apoptosis.
Does Leishmaniasis disease alter the parenchyma and protein expression in salivary glands?
da Silva et al., Teresina, Brazil. In Exp Biol Med (maywood), Dec 2015
After 50 days, animals were euthanized and major salivary glands were collected to perform histological, immunohistochemical and epifluorescence techniques using anti-Caspase-2, anti-Ki-67 and anti-β-catenin antibodies, respectively.
Stressed-Out Endoplasmic Reticulum Inflames the Mitochondria.
Argon et al., Philadelphia, United States. In Immunity, Oct 2015
(2015) show that during Brucella abortus infection, an endoplasmic reticulum stress sensor, IRE1α, initiates NLRP3- and caspase-2-mediated mitochondrial damage that potentiates NLRP3 inflammasome assembly.
Endoplasmic Reticulum Stress Activates the Inflammasome via NLRP3- and Caspase-2-Driven Mitochondrial Damage.
O'Riordan et al., Ann Arbor, United States. In Immunity, Oct 2015
NLRP3 was required for ER stress-induced cleavage of caspase-2 and the pro-apoptotic factor, Bid, leading to subsequent release of mitochondrial contents.
Poly(ADP-ribose) in the bone: from oxidative stress signal to structural element.
Virág et al., Debrecen, Hungary. In Free Radic Biol Med, May 2015
In the past decades numerous studies demonstrating production of reactive oxygen or nitrogen intermediates, effects of different antioxidants, and involvement of prototypical redox control mechanisms (Nrf2-Keap1, Steap4, FoxO, PAMM, caspase-2) have proven the central role of redox regulation in the bone.
Caspase-2: the reinvented enzyme.
Zhivotovsky et al., Stockholm, Sweden. In Oncogene, May 2015
On the basis of evidences that caspase-2 gene targeting in several generated mouse models accelerates tumor formation, this enzyme was recently implicated in tumor suppression.
Old, new and emerging functions of caspases.
Kumar et al., Adelaide, Australia. In Cell Death Differ, Apr 2015
Notable among them are caspase-2, -8 and -14.
Inhibition of NF-κB by deoxycholic acid induces miR-21/PDCD4-dependent hepatocelular apoptosis.
E Castro et al., Lisbon, Portugal. In Sci Rep, 2014
In turn, DCA-induced oxidative stress resulted in caspase-2 activation and NF-κB/miR-21 inhibition, in a PIDD-dependent manner.
Caspase-2 as a tumour suppressor.
Kumar et al., Adelaide, Australia. In Cell Death Differ, 2013
Ever since its discovery 20 years ago, caspase-2 has been enigmatic and its function somewhat controversial.
[Caspase-2: what do we know today?].
Lavrik et al., In Mol Biol (mosk), 2013
This review is focused on various mechanisms of signal transduction through caspase-2 which believed to be one of the most enigmatical protease involved in apoptosis.
Neuronal caspase 2 activity and function requires RAIDD, but not PIDD.
Troy et al., New York City, United States. In Biochem J, 2012
Activation of neuronal Casp2 and induction of this activity depends on expression of receptor-interacting protein RAIDD, but is independent of p53-inducible protein with a death domain (PIDD) expression.
Caspase-2 is an initiator caspase responsible for pore-forming toxin-mediated apoptosis.
Rajalingam et al., Frankfurt am Main, Germany. In Embo J, 2012
These results revealed a thus far unknown, obligatory role for caspase-2 as an initiator caspase during pore-forming toxins -mediated apoptosis.
Combined effect of hypothermia and caspase-2 gene deficiency on neonatal hypoxic-ischemic brain injury.
Hagberg et al., Göteborg, Sweden. In Pediatr Res, 2012
caspase-2 gene deficiency combined with hypothermia provided enhanced neuroprotection as compared with hypothermia alone
Tumor-suppressing function of caspase-2 requires catalytic site Cys-320 and site Ser-139 in mice.
Du et al., Cincinnati, United States. In J Biol Chem, 2012
Tumor-suppressing function of caspase-2 requires catalytic site Cys-320 and site Ser-139 in mice.
TAp73alpha protects small cell lung carcinoma cells from caspase-2 induced mitochondrial mediated apoptotic cell death.
Joseph et al., Stockholm, Sweden. In Oncotarget, 2011
TAp73alpha represses caspase-2 enzymatic activity and by this means reduce caspase-2 induced Bax activation, loss of mitochondrial transmembrane potential and resulting apoptosis in small cell lung carcinoma cells.
Virus-tumor interactome screen reveals ER stress response can reprogram resistant cancers for oncolytic virus-triggered caspase-2 cell death.
Stojdl et al., Ottawa, Canada. In Cancer Cell, 2011
Further investigation revealed an unconventional mechanism whereby ER stress response inhibition preconditioned cancer cells, which sensitized them to caspase-2-dependent apoptosis induced by a subsequent rhabdovirus infection.
Meeting the (N-terminal) end with acetylation.
Kornbluth et al., Durham, United States. In Cell, 2011
In this issue, Yi et al. (2011) introduce a mechanism by which Bcl-xL lowers the threshold for apoptosis by suppressing acetyl-CoA production, which, in turn, suppresses the N-alpha-acetylation important for activation of the proapoptotic protease caspase-2.
The engine driving the ship: metabolic steering of cell proliferation and death.
Kornbluth et al., Durham, United States. In Nat Rev Mol Cell Biol, 2010
D-type cyclins, cyclin-dependent kinases, the anaphase-promoting complex, p53, caspase 2 and B cell lymphoma 2 proteins, among others, have been shown to be regulated by metabolic crosstalk.
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