Caspase 12

A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 12 is activated by pro-apoptotic factors that are released during cell stress and by CARD SIGNALING ADAPTOR PROTEINS. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.

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Networked: 290 relevant articles (8 outcomes, 25 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Saleh, Maya: 8 articles (01/2016 - 05/2004)
2.	Wang, Wan-Tie: 5 articles (04/2018 - 09/2014)
3.	Han, Fang: 5 articles (08/2015 - 01/2013)
4.	Shi, Yuxiu: 4 articles (12/2021 - 07/2013)
5.	Nicholson, Donald W: 4 articles (06/2009 - 05/2004)
6.	Li, Ying: 3 articles (12/2022 - 06/2009)
7.	Zhang, Chengcheng: 3 articles (01/2021 - 01/2017)
8.	Ying, Lei: 3 articles (04/2018 - 09/2014)
9.	Xiang, Bing-Qian: 3 articles (08/2017 - 02/2016)
10.	Chien, Chiang-Ting: 3 articles (01/2015 - 01/2010)

Related Diseases

1.	Myocardial Infarction 12/01/2020 - "To investigate the therapeutic and diagnostic value of caspase-12 and study of growth differentiation factor-15 (GDF-15) in patients with acute myocardial infarction (AMI). " 09/01/2011 - "The results suggest that EPO improves heart function in myocardial infarction rats by down-regulating the expression of caspase-12, which may protect the myocardium by abrogating endoplasmic reticulum stress-mediated cardiomyocyte apoptosis and improving heart function." 09/01/2011 - "The expression of caspase-12 in the myocardial infarction group was also increased compared to the EPO treatment group rats. " 09/01/2011 - "In the present study, the myocardial protective effects of erythropoietin (EPO) by inhibition of the expression of caspase-12 were investigated in a myocardial infarction rat model. " 09/01/2011 - "Protective effect of erythropoietin on myocardial infarction in rats by inhibition of caspase-12 expression."
2.	Hypoxia (Hypoxemia) 01/01/2018 - "Knockdown of caspase-4, an alternative to caspase-12 in humans, markedly alleviated CRHT2 activation-induced apoptosis in human cardiomyocyte response to anoxia. " 10/25/2006 - "Using primary cultured neonatal cardiomyocytes, CRT and caspase-12 expression and activation during hypoxic preconditioning (HPC) and hypoxia/reoxygenation (H/R) were studied to explore the role of ERS in cardioprotection by HPC. " 11/01/2005 - "We found that hypoxia induced ER stress, as assessed by the expression of CHOP and BiP and cleavage of caspase 12. " 02/01/2021 - "In conclusion, treatment with 1 µM DEX alleviated cell injury, apoptosis and the increases in GRP78, CHOP and caspase-12 expression levels in H9c2 cells induced by 3 h of hypoxia and 3 h of reoxygenation." 08/25/2017 - "To investigate the effects of dexmedetomidine (DEX) on hypoxia/reoxygenation (H/R) injury-induced cell apoptosis and caspase-12 expression, A549 cells were randomly divided into 4 groups: control group, DEX group, H/R group and DEX+H/R group. "
3.	Infarction (Infarctions) 12/01/2020 - "Therapeutic and Diagnostic Value of Caspase-12 and Study of Growth Differentiation Factor-15 in Patients with Acute Myocar-dial Infarction." 01/09/2012 - "Rats were sacrificed 24h later; infarct volumes were measured, and Bax, Bcl-2, TUNEL and caspase-12 immunostaining was evaluated. " 07/01/2011 - "Our findings reveal that caspase-12 is fragmented when infarct areas form in cerebral cortical neurons. " 01/01/2012 - "The results showed that during the reperfusion period following 45 min of coronary ligation the infarct size (IS) increased from 3 h of reperfusion (45.4±5.57%) to 24 h reperfusion (64.21±5.43, P<0.05), which was associated with ER stress dependent apoptosis signaling activation including CHOP, Caspase-12 and JNK (P<0.05, respectively).The dynamic ER stress activation was also related to impaired SERCA activity at 24 h of reperfusion. " 07/01/2015 - "Furthermore, the results showed that treatment with salubrinal can decrease cardiomyocyte apoptosis and infarct size by increasing eIF2α phosphorylation and decreasing the expression of caspase-12 and CHOP. "
4.	Wounds and Injuries (Trauma) 08/25/2017 - "In addition, there was a significant negative correlation between myocardial caspase-12 activity and trauma-induced secondary cardiac dysfunction. " 08/25/2017 - "Activation of caspase-12 at early stage contributes to cardiomyocyte apoptosis in trauma-induced secondary cardiac injury." 02/08/2016 - "DEX can effectively relieve the lung I/R injuries in mice, which maybe associated with inhibition of pneumocyte apoptosis induced by ERS-related Caspase-12 pathway." 06/01/2009 - "It may be related with cellular injuries induced by caspase-12 apoptotic pathways through activated endoplasmic reticulum stress." 08/25/2017 - "The activity and expression of caspase-12, an endoplasmic reticulum (ER) stress-specific caspase, elevated markedly 3 h after trauma and reached its peak 6 h after trauma. "
5.	Cardiomyopathies (Cardiomyopathy) 02/01/2008 - "This reduced not only the increase of cleaved caspase-12 but also of the number of myocyte apoptosis produced by beta(1)-EC(II) IgG. Thus, we conclude that ER stress plays an important role in cell death and cardiac dysfunction in beta(1)-EC(II) IgG cardiomyopathy, and the effects of beta(1)-EC(II) IgG are mediated via the beta(1)-adrenergic receptor." 01/01/2015 - "Shengmai injection improved doxorubicin-induced cardiomyopathy by alleviating myocardial endoplasmic reticulum stress and caspase-12 dependent apoptosis."

Related Drugs and Biologics

1.	Proteins (Proteins, Gene)
2.	Endoplasmic Reticulum Chaperone BiP
3.	Caspase 3 (Caspase-3)
4.	Caspase 9
5.	Erythropoietin
6.	Messenger RNA (mRNA)
7.	4-phenylbutylamine
8.	L-Lactate Dehydrogenase (Lactate Dehydrogenase)
9.	Growth Differentiation Factor 15
10.	NAD (NADH)

Related Therapies and Procedures

1.	Electroacupuncture
2.	Transplantation
3.	Therapeutics
4.	CHOP-B protocol
5.	Operative Surgical Procedures