B6.129P2-Txnrd1tm1Marc/Ieg

Status

Available to order

EMMA IDEM:05844
Citation informationRRID:IMSR_EM:05844 

Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information.

International strain nameB6.129P2-Txnrd1tm1Marc/Ieg
Alternative nameTxnrd1tm1Marc (thioredoxin reductase 1)
Strain typeTargeted Mutant Strains : Conditional mutation
Allele/Transgene symbolTxnrd1tm1Marc
Gene/Transgene symbolTxnrd1

Information from provider

ProviderMarcus Conrad
Provider affiliationInstitut of Clinical Molecular Biology and Tumor Genetics, Helmholtz Zentrum Muenchen
Genetic informationExon 15, which encodes 22 amino acids and the C-terminally located redox center consisting of Gly-Cys-Sec-Gly of Txnrd1, and 1.7 kb of the 3' UTR containing the selenocysteine insertion element, essential for cotranslational Sec incorporation at the UGA codon, AU-rich mRNA instability elements and the endogenous transcription stop signal, were flanked by loxP sites. Cre-mediated removal of the last exon leads to a dysfunctional Txnrd1 allele.
Phenotypic informationUbiquitous Cre-mediated removal of both Txnrd1 causes early embryonic death between E8.5 and E9.5 due to severe overall growth and developmental retardation. Heart-specific Txnrd1 deletion does not cause any overt impairment of cardiac development and function, whereas central-nervous system specific Txnrd1 inactivation causes massive cerebellar hypoplasia and ataxia.
Breeding historyMore than 10 generations backcrossed on C57BL/6.
References
  • Cytoplasmic thioredoxin reductase is essential for embryogenesis but dispensable for cardiac development.;Jakupoglu Cemile, Przemeck Gerhard K H, Schneider Manuela, Moreno Stéphanie G, Mayr Nadja, Hatzopoulos Antonis K, de Angelis Martin Hrabé, Wurst Wolfgang, Bornkamm Georg W, Brielmeier Markus, Conrad Marcus, ;2005;Molecular and cellular biology;25;1980-8; 15713651
  • The role of thioredoxin reductases in brain development.;Soerensen Jonna, Jakupoglu Cemile, Beck Heike, Förster Heidi, Schmidt Jörg, Schmahl Wolfgang, Schweizer Ulrich, Conrad Marcus, Brielmeier Markus, ;2008;PloS one;3;e1813; 18350150
  • Mitochondrial thioredoxin reductase is essential for early postischemic myocardial protection.;Horstkotte Jan, Perisic Tamara, Schneider Manuela, Lange Philipp, Schroeder Melanie, Kiermayer Claudia, Hinkel Rabea, Ziegler Tilman, Mandal Pankaj K, David Robert, Schulz Sabine, Schmitt Sabine, Widder Julian, Sinowatz Fred, Becker Bernhard F, Bauersachs Johann, Naebauer Michael, Franz Wolfgang M, Jeremias Irmela, Brielmeier Markus, Zischka Hans, Conrad Marcus, Kupatt Christian, ;2011;Circulation;124;2892-902; 22144571
  • System x(c)- and thioredoxin reductase 1 cooperatively rescue glutathione deficiency.;Mandal Pankaj Kumar, Seiler Alexander, Perisic Tamara, Kölle Pirkko, Banjac Canak Ana, Förster Heidi, Weiss Norbert, Kremmer Elisabeth, Lieberman Michael W, Bannai Shiro, Kuhlencordt Peter, Sato Hideyo, Bornkamm Georg W, Conrad Marcus, ;2010;The Journal of biological chemistry;285;22244-53; 20463017
  • Loss of thioredoxin reductase 1 renders tumors highly susceptible to pharmacologic glutathione deprivation.;Mandal Pankaj Kumar, Schneider Manuela, Kölle Pirkko, Kuhlencordt Peter, Förster Heidi, Beck Heike, Bornkamm Georg W, Conrad Marcus, ;2010;Cancer research;70;9505-14; 21045148
Homozygous fertileyes
Homozygous viableyes
Homozygous matings requiredno
Immunocompromisedno

Information from EMMA

Archiving centreHelmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH), Oberschleißheim, Germany

Disease and phenotype information

MGI phenotypes (gene matching)
  • decreased cell proliferation / MGI
  • failure of primitive streak formation / MGI
  • failure to gastrulate / MGI
  • decreased embryo size / MGI
  • abnormal visceral yolk sac morphology / MGI
  • embryonic growth arrest / MGI
  • abnormal embryonic tissue morphology / MGI
  • abnormal neural tube morphology / MGI
  • no abnormal phenotype detected / MGI
  • failure of initiation of embryo turning / MGI
  • increased trophoblast giant cell number / MGI
  • impaired somite development / MGI
  • embryonic lethality between somite formation and embryo turning, complete penetrance / MGI
  • embryonic lethality during organogenesis, complete penetrance / MGI
  • absent embryonic epiblast / MGI
  • abnormal visceral endoderm morphology / MGI
  • absent fibroblast proliferation / MGI
  • short rostral-caudal axis / MGI

Literature references

  • Cytoplasmic thioredoxin reductase is essential for embryogenesis but dispensable for cardiac development.;Jakupoglu Cemile, Przemeck Gerhard K H, Schneider Manuela, Moreno Stéphanie G, Mayr Nadja, Hatzopoulos Antonis K, de Angelis Martin Hrabé, Wurst Wolfgang, Bornkamm Georg W, Brielmeier Markus, Conrad Marcus, ;2005;Molecular and cellular biology;25;1980-8; 15713651
  • The role of thioredoxin reductases in brain development.;Soerensen Jonna, Jakupoglu Cemile, Beck Heike, Förster Heidi, Schmidt Jörg, Schmahl Wolfgang, Schweizer Ulrich, Conrad Marcus, Brielmeier Markus, ;2008;PloS one;3;e1813; 18350150
  • Mitochondrial thioredoxin reductase is essential for early postischemic myocardial protection.;Horstkotte Jan, Perisic Tamara, Schneider Manuela, Lange Philipp, Schroeder Melanie, Kiermayer Claudia, Hinkel Rabea, Ziegler Tilman, Mandal Pankaj K, David Robert, Schulz Sabine, Schmitt Sabine, Widder Julian, Sinowatz Fred, Becker Bernhard F, Bauersachs Johann, Naebauer Michael, Franz Wolfgang M, Jeremias Irmela, Brielmeier Markus, Zischka Hans, Conrad Marcus, Kupatt Christian, ;2011;Circulation;124;2892-902; 22144571
  • System x(c)- and thioredoxin reductase 1 cooperatively rescue glutathione deficiency.;Mandal Pankaj Kumar, Seiler Alexander, Perisic Tamara, Kölle Pirkko, Banjac Canak Ana, Förster Heidi, Weiss Norbert, Kremmer Elisabeth, Lieberman Michael W, Bannai Shiro, Kuhlencordt Peter, Sato Hideyo, Bornkamm Georg W, Conrad Marcus, ;2010;The Journal of biological chemistry;285;22244-53; 20463017
  • Loss of thioredoxin reductase 1 renders tumors highly susceptible to pharmacologic glutathione deprivation.;Mandal Pankaj Kumar, Schneider Manuela, Kölle Pirkko, Kuhlencordt Peter, Förster Heidi, Beck Heike, Bornkamm Georg W, Conrad Marcus, ;2010;Cancer research;70;9505-14; 21045148

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