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

Caspase 12

cysteine-aspartic acid protease (caspase); involved with the terminal stage of apoptosis [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: PrP, GRP78, CHOP, caspase-3, V1a
Papers using caspase-12 antibodies
Endoplasmic reticulum stress inhibition protects against excitotoxic neuronal injury in the rat brain
Wu Jang-Yen et al., In Journal of Biomedical Science, 2006
... Mouse anti-actin, rabbit anti-GRP78, rabbit anti-CHOP/GADD153, rabbit anti-caspase-12 antibodies and secondary mouse and rabbit antibodies were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA) ...
Cross-talk in cell death signaling
Bose S et al., In Cancer gene therapy, 1999
... Caspase-12 inhibitor (Z-ATAD-FMK) was purchased from MBL.
Cadmium-mediated oxidative stress in kidney proximal tubule cells induces degradation of Na+/K+-ATPase through proteasomal and endo−/lysosomal proteolytic pathways.
Maki Carl G., In PLoS ONE, 1998
... (PARP), caspase 12, and caspase 3 antibodies were purchased from Cell Signaling Technology (Beverly, MA); the anti-caspase 12 antibody was purchased from Abcam (Cambridge, MA); and the ...
Persistent activation of RelA by respiratory syncytial virus involves protein kinase C, underphosphorylated IkappaB-beta, and sequestration of protein phosphatase 2A by the viral phosphoprotein
Barik Sailen et al., In BMC Microbiology, 1997
... Sp1 (Santa Cruz Biotechnology); phospho-AKT, caspases-3, -6, -7, -8, -9 (Cell Signaling Technology); caspase-10 (Oncogene); caspase-12 (Sigma); IκB-α (Biomol); nonerythroid alpha-spectrin (Chemicon International); ...
Papers on caspase-12
Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress.
Chen et al., Guangzhou, China. In Acta Pharmacol Sin, Feb 2016
Meanwhile, SFN significantly alleviated the damage of ΔΨm and decreased the expression of ER stress-related apoptosis proteins (GRP78, CHOP and caspase-12), elevating the expression of SIRT1 and Bcl-2/Bax ratio in the cardiomyocytes.
Involvement of Endoplasmic Reticulum Stress in Uremic Cardiomyopathy: Protective Effects of Tauroursodeoxycholic Acid.
Gu et al., Shanghai, China. In Cell Physiol Biochem, Feb 2016
ERS markers (GRP78, GRP94, P-PERK, P-eIF2a) and ERS-induced apoptosis pathways (activation of CHOP and caspase-12) were increased significantly in 5/6 nephrectomy mice, and TUDCA treatment blunted these changes.
Salidroside Protects Against 6-Hydroxydopamine-Induced Cytotoxicity by Attenuating ER Stress.
Yang et al., Xi'an, China. In Neurosci Bull, Feb 2016
Furthermore, treatment of a DA neuronal cell line (SN4741) and primary cortical neurons with salidroside significantly reduced neurotoxin-induced increases in cytoplasmic reactive oxygen species and calcium, both of which cause ER stress, and cleaved caspase-12, which is responsible for ER stress-induced cell death.
Excessive Selenium Supplementation Induced Oxidative Stress and Endoplasmic Reticulum Stress in Chicken Spleen.
He et al., Mianyang, China. In Biol Trace Elem Res, Feb 2016
Then, the levels of antioxidative enzymes, GPx, SOD, and MDA as well as the expression levels of GRP78, ARF6, caspase 3, caspase 12, and Bcl 2 in the spleen were determined at days 15, 30, and 45, respectively.
ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction underlie apoptosis induced by resveratrol and arsenic trioxide in A549 cells.
Zhang et al., Chengdu, China. In Chem Biol Interact, Feb 2016
Then, we demonstrated that ER stress was contributed to this synergistic effect, which was manifested by increased the expression levels of ER stress hallmarks, including 78-kDa glucose-regulated protein (GRP 78), caspase 12 and C/EBP-homologous protein (CHOP), In addition, mitochondrial dysfunction was observed after exposure of A549 cells to resveratrol or/and ATO, which was displayed by some alterations of mitochondria-related events, such as loss of mitochondrial membrane potential, cytochrome c release and changes of Bax and Bcl-2 expressions.
Mechanisms of interaction of the N-acetyl-p-aminophenol metabolites in terms of nephrotoxicity.
Milnerowicz et al., Wrocław, Poland. In Drug Chem Toxicol, Apr 2015
N-acetyl-p-aminophenol may initiate the apoptosis process involving activation of caspase-9 and caspase-3, but also caspase-12 as a result of generation of free radicals.
Inflammatory caspases: key regulators of inflammation and cell death.
Lamkanfi et al., In Biol Chem, Mar 2015
Although the immune roles of caspase-12 are debated, it was proposed to dampen inflammatory responses by interfering with caspase-1 activation and other innate immune pathways.
Synthetic lethal metabolic targeting of cellular senescence in cancer therapy.
Schmitt et al., Berlin, Germany. In Nature, 2013
Accordingly, TIS lymphomas, unlike senescence models that lack a strong SASP response, were more sensitive to blocking glucose utilization or autophagy, which led to their selective elimination through caspase-12- and caspase-3-mediated endoplasmic-reticulum-related apoptosis.
Regulation of apoptosis in adipocytes and breast cancer cells by 1,25-dihydroxyvitamin D3: a link between obesity and breast cancer.
Sergeev, Brookings, United States. In Horm Mol Biol Clin Investig, 2013
This signal acts as an apoptotic initiator that directly recruits Ca2+-dependent apoptotic effectors, calpain and caspase 12, in breast cancer cells and adipocytes.
Signaling pathways involved in endoplasmic reticulum stress-induced neuronal apoptosis.
Yin et al., Beijing, China. In Int J Neurosci, 2013
However, chronic or unresolved ER stress can induce neuronal apoptosis by activating c-Jun N-terminal kinase (JNK), glycogen synthase kinase 3/3β (GSK3/3β), CAAT/enhancer binding protein homologous protein (CHOP), and caspase-12 pathway.
Complex roles of caspases in the pathogenesis of inflammatory bowel disease.
Neurath et al., Erlangen, Germany. In Gastroenterology, 2013
In particular, caspase-1, caspase-4, caspase-5, and caspase-12 are activated during innate immune responses and participate in the formation of the inflammasome.
The nephroprotective effect of tauroursodeoxycholic acid on ischaemia/reperfusion-induced acute kidney injury by inhibiting endoplasmic reticulum stress.
Mei et al., China. In Basic Clin Pharmacol Toxicol, 2012
Tauroursodeoxycholic acid intervention down-regulated GRP78 and CHOP expression and Caspase 12 activation.
Reactive oxygen species-triggered trophoblast apoptosis is initiated by endoplasmic reticulum stress via activation of caspase-12, CHOP, and the JNK pathway in Toxoplasma gondii infection in mice.
Shen et al., Hefei, China. In Infect Immun, 2012
It was concluded that apoptosis in placental trophoblasts was initiated predominantly by ROS-mediated ERS via activation of caspase-12, CHOP, and the JNK pathway in acute T. gondii infection.
Mild hypothermia enhanced the protective effect of protein therapy with transductive anti-death FNK protein using a rat focal transient cerebral ischemia model.
Katayama et al., Tokyo, Japan. In Brain Res, 2012
The protective mechanisms of fused FNK protein therapy might involve the inhibition of apoptotic pathways through caspase-12, but not through Bcl-2.
Induction of the intrinsic apoptosis pathway in insulin-secreting cells is dependent on oxidative damage of mitochondria but independent of caspase-12 activation.
Lortz et al., Hannover, Germany. In Biochim Biophys Acta, 2011
Mitochondrial caspase-9 is not a downstream substrate of endoplasmic reticulum-specific caspase-12 .
Induction of ER stress in response to oxygen-glucose deprivation of cortical cultures involves the activation of the PERK and IRE-1 pathways and of caspase-12.
Rodríguez-Alvarez et al., Barcelona, Spain. In Cell Death Dis, 2010
Processing of procaspase-12 was mediated by NMDA receptor and calpain activation
Caspase-12 controls West Nile virus infection via the viral RNA receptor RIG-I.
Fikrig et al., New Haven, United States. In Nat Immunol, 2010
Caspase-12 was required for an effective antiviral immune response, especially for the production of type I interferons through the regulation of TRIM25-mediated ubiquitination of RIG-I. .
Enhanced bacterial clearance and sepsis resistance in caspase-12-deficient mice.
Nicholson et al., San Diego, United States. In Nature, 2006
In mice, caspase-12 deficiency confers resistance to sepsis and its presence exerts a dominant-negative suppressive effect on caspase-1, resulting in enhanced vulnerability to bacterial infection and septic mortality
Differential modulation of endotoxin responsiveness by human caspase-12 polymorphisms.
Nicholson et al., Montréal, Canada. In Nature, 2004
Although caspase-12 is phylogenetically related to the cytokine maturation caspases, in mice it has been proposed as a mediator of apoptosis induced by endoplasmic reticulum stress including amyloid-beta cytotoxicity, suggesting that it might contribute to the pathogenesis of Alzheimer's disease.
Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta.
Yuan et al., Boston, United States. In Nature, 2000
Here we show that caspase-12 is localized to the ER and activated by ER stress, including disruption of ER calcium homeostasis and accumulation of excess proteins in ER, but not by membrane- or mitochondrial-targeted apoptotic signals.
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