Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10366)
Regulator Name Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1)
Synonyms
MALT lymphoma-associated translocation
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Gene Name MALT1
Gene ID 10892
Regulator Type Protein coding
Uniprot ID Q9UDY8
Sequence
MSLLGDPLQALPPSAAPTGPLLAPPAGATLNRLREPLLRRLSELLDQAPEGRGWRRLAEL
AGSRGRLRLSCLDLEQCSLKVLEPEGSPSLCLLKLMGEKGCTVTELSDFLQAMEHTEVLQ
LLSPPGIKITVNPESKAVLAGQFVKLCCRATGHPFVQYQWFKMNKEIPNGNTSELIFNAV
HVKDAGFYVCRVNNNFTFEFSQWSQLDVCDIPESFQRSVDGVSESKLQICVEPTSQKLMP
GSTLVLQCVAVGSPIPHYQWFKNELPLTHETKKLYMVPYVDLEHQGTYWCHVYNDRDSQD
SKKVEIIIGRTDEAVECTEDELNNLGHPDNKEQTTDQPLAKDKVALLIGNMNYREHPKLK
APLVDVYELTNLLRQLDFKVVSLLDLTEYEMRNAVDEFLLLLDKGVYGLLYYAGHGYENF
GNSFMVPVDAPNPYRSENCLCVQNILKLMQEKETGLNVFLLDMCRKRNDYDDTIPILDAL
KVTANIVFGYATCQGAEAFEIQHSGLANGIFMKFLKDRLLEDKKITVLLDEVAEDMGKCH
LTKGKQALEIRSSLSEKRALTDPIQGTEYSAESLVRNLQWAKAHELPESMCLKFDCGVQI
QLGFAAEFSNVMIIYTSIVYKPPEIIMCDAYVTDFPLDLDIDPKDANKGTPEETGSYLVS
KDLPKHCLYTRLSSLQKLKEHLVFTVCLSYQYSGLEDTVEDKQEVNVGKPLIAKLDMHRG
LGRKTCFQTCLMSNGPYQSSAATSGGAGHYHSLQDPFHGVYHSHPGNPSNVTPADSCHCS
RTPDAFISSFAHHASCHFSRSNVPVETTDEIPFSFSDRLRISEK

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Family Peptidase C14B family
Function
Protease that enhances BCL10-induced activation: acts via formation of CBM complexes that channel adaptive and innate immune signaling downstream of CARD domain-containing proteins (CARD9, CARD11 and CARD14) to activate NF-kappa-B and MAP kinase p38 pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Mediates BCL10 cleavage: MALT1-dependent BCL10 cleavage plays an important role in T-cell antigen receptor-induced integrin adhesion. Involved in the induction of T helper 17 cells (Th17) differentiation. Cleaves RC3H1 and ZC3H12A in response to T-cell receptor (TCR) stimulation which releases their cooperatively repressed targets to promote Th17 cell differentiation. Also mediates cleavage of N4BP1 in T-cells following TCR-mediated activation, leading to N4BP1 inactivation. May also have ubiquitin ligase activity: binds to TRAF6, inducing TRAF6 oligomerization and activation of its ligase activity.

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HGNC ID
HGNC:6819
KEGG ID hsa:10892
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
MALT1 can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
Browse Target
Browse Disease
Browse Drug
Nuclear factor erythroid 2-related factor 2 (NFE2L2) [Suppressor; Marker]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Marker/Suppressor
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Responsed Drug Micafungin Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
The surgical procedure for establishing the myocardial I/R injury rat model was carried out as we did before. Briefly, a left thoracotomy was performed in the fourth intercostal space and the heart was exposed via opening thepericardium. The left coronary artery was surrounded with a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion. At the end, the blood and hearts were collected for assay of the creatine kinase(CK) activity and infarct size to determine the success of I/R injury model. To explore the role of MALT1 in myocardial I/R injury the underlying mechanisms, three sets of experiment were performed.

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Response regulation The inhibition of MALT1 can reduce ischemia/reperfusion-induced myocardial ferroptosis through enhancing the Nrf2/SLC7A11 pathway; and MALT1 may be used as a potential target to seek novel or existing drugs (such as micafungin) for treating myocardial infarction.
Cystine/glutamate transporter (SLC7A11) [Driver; Suppressor]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Suppressor
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Responsed Drug Micafungin Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
The surgical procedure for establishing the myocardial I/R injury rat model was carried out as we did before. Briefly, a left thoracotomy was performed in the fourth intercostal space and the heart was exposed via opening thepericardium. The left coronary artery was surrounded with a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion. At the end, the blood and hearts were collected for assay of the creatine kinase(CK) activity and infarct size to determine the success of I/R injury model. To explore the role of MALT1 in myocardial I/R injury the underlying mechanisms, three sets of experiment were performed.

    Click to Show/Hide
Response regulation The inhibition of MALT1 can reduce ischemia/reperfusion-induced myocardial ferroptosis through enhancing the Nrf2/SLC7A11 pathway; and MALT1 may be used as a potential target to seek novel or existing drugs (such as micafungin) for treating myocardial infarction.
Ischemia/reperfusion injury [ICD-11: DB98]
 Disease Info 
In total 2 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) Protein coding
 Regulator Info 
Responsed Drug Micafungin Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
The surgical procedure for establishing the myocardial I/R injury rat model was carried out as we did before. Briefly, a left thoracotomy was performed in the fourth intercostal space and the heart was exposed via opening thepericardium. The left coronary artery was surrounded with a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion. At the end, the blood and hearts were collected for assay of the creatine kinase(CK) activity and infarct size to determine the success of I/R injury model. To explore the role of MALT1 in myocardial I/R injury the underlying mechanisms, three sets of experiment were performed.

    Click to Show/Hide
Response regulation The inhibition of MALT1 can reduce ischemia/reperfusion-induced myocardial ferroptosis through enhancing the Nrf2/SLC7A11 pathway; and MALT1 may be used as a potential target to seek novel or existing drugs (such as micafungin) for treating myocardial infarction.
Experiment 2 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) Protein coding
 Regulator Info 
Responsed Drug Micafungin Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
The surgical procedure for establishing the myocardial I/R injury rat model was carried out as we did before. Briefly, a left thoracotomy was performed in the fourth intercostal space and the heart was exposed via opening thepericardium. The left coronary artery was surrounded with a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion. At the end, the blood and hearts were collected for assay of the creatine kinase(CK) activity and infarct size to determine the success of I/R injury model. To explore the role of MALT1 in myocardial I/R injury the underlying mechanisms, three sets of experiment were performed.

    Click to Show/Hide
Response regulation The inhibition of MALT1 can reduce ischemia/reperfusion-induced myocardial ferroptosis through enhancing the Nrf2/SLC7A11 pathway; and MALT1 may be used as a potential target to seek novel or existing drugs (such as micafungin) for treating myocardial infarction.
Micafungin [Investigative]
 Drug Info 
In total 2 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Nuclear factor erythroid 2-related factor 2 (NFE2L2) Suppressor; Marker
 Target Info 
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
The surgical procedure for establishing the myocardial I/R injury rat model was carried out as we did before. Briefly, a left thoracotomy was performed in the fourth intercostal space and the heart was exposed via opening thepericardium. The left coronary artery was surrounded with a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion. At the end, the blood and hearts were collected for assay of the creatine kinase(CK) activity and infarct size to determine the success of I/R injury model. To explore the role of MALT1 in myocardial I/R injury the underlying mechanisms, three sets of experiment were performed.

    Click to Show/Hide
Response regulation The inhibition of MALT1 can reduce ischemia/reperfusion-induced myocardial ferroptosis through enhancing the Nrf2/SLC7A11 pathway; and MALT1 may be used as a potential target to seek novel or existing drugs (such as micafungin) for treating myocardial infarction.
Experiment 2 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Cystine/glutamate transporter (SLC7A11) Driver; Suppressor
 Target Info 
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Pathway Response Ferroptosis hsa04216
Fatty acid metabolism hsa01212
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
The surgical procedure for establishing the myocardial I/R injury rat model was carried out as we did before. Briefly, a left thoracotomy was performed in the fourth intercostal space and the heart was exposed via opening thepericardium. The left coronary artery was surrounded with a 4-0 silk suture and a snare was formed by passing both ends of the suture via a short polyethylene tubing. Blockage of the coronary artery was conducted via clamping the snare against the heart surface. Reperfusion was performed by release of the snare. The sham group conducted the same procedure but without ischemia (the snare was not tightened). To establish the I/R injury model, the rat hearts were subjected to 1 h-ischemia plus 3 h-reperfusion. At the end, the blood and hearts were collected for assay of the creatine kinase(CK) activity and infarct size to determine the success of I/R injury model. To explore the role of MALT1 in myocardial I/R injury the underlying mechanisms, three sets of experiment were performed.

    Click to Show/Hide
Response regulation The inhibition of MALT1 can reduce ischemia/reperfusion-induced myocardial ferroptosis through enhancing the Nrf2/SLC7A11 pathway; and MALT1 may be used as a potential target to seek novel or existing drugs (such as micafungin) for treating myocardial infarction.
References
Ref 1 Inhibition of MALT1 reduces ferroptosis in rat hearts following ischemia/reperfusion via enhancing the Nrf2/SLC7A11 pathway. Eur J Pharmacol. 2023 Jul 5;950:175774. doi: 10.1016/j.ejphar.2023.175774. Epub 2023 May 3.