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Early Embryonic Lethality Caused by Targeted Disruption of the Mouse Thioredoxin Gene
Open accessAbstract
Thioredoxins belong to a widely distributed group of small proteins with strong reducing activities mediated by a consensus redox-active dithiol (Cys-Gly-Pro-Cys). Thioredoxin was first isolated as a hydrogen donor for enzymatic synthesis of deoxyribonucleotides by ribonucleotide reductase in Escherichia coli. Recent studies have revealed a variety of roles that thioredoxin plays in transcription, growth control, and immune function. In this report, we describe the phenotype of mice carrying a targeted disruption of the thioredoxin gene (Txn). Heterozygotes are viable, fertile, and appear normal. In contrast, homozygous mutants die shortly after implantation, and the concepti were resorbed prior to gastrulation. When preimplantation embryos were placed in culture, the inner cell mass cells of the homozygous embryos failed to proliferate. These results indicate that Txn expression is essential for early differentiation and morphogenesis of the mouse embryo.
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“Both Trx1 and Trx2 appear to be essential, as complete deficiency of either subtype causes early embryonic lethality in mice (280, 317).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [280]
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“Conversely, embryonic lethality of mice lacking either Txn1 (Matsui et al., 1996) or Txnrd1 (Bondareva et al., 2007; Jakupoglu et al., 2005) indicates that some aspect of the Txnrd1-dependent pathway is essential in mammals.”
BackgroundInfluentialThe paradoxical role of thioredoxin on oxidative stress and aging
Cunningham, G. M., Roman, M. G., Flores, L. C., Hubbard, G. B., Salmon, A. B., Zhang, Y., Gelfond, J., & Ikeno, Y. (2015) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2015.02.025 · Cited by 61
Cunning factor: macrophage migration inhibitory factor as a redox‐regulated target
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Thioredoxin-1 and Endothelial Cell Aging: Role in Cardiovascular Diseases
Altschmied, J., & Haendeler, J. (2009) · Antioxidants and Redox Signaling · doi:10.1089/ars.2008.2379 · Cited by 62
“Genetic targeting of Trx-1 leads to a lethal phenotype (34).”
Nuclear Translocation of Nuclear Factor Kappa B in Early 1-Cell Mouse Embryos1
Nishikimi, A., Mukai, J., & Yamada, M. (1999) · Biology of Reproduction · doi:10.1095/biolreprod60.6.1536 · Cited by 55
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“With the development of technologies for targeted gene disruption, many essential genes were identified by studying single gene functions in murine knockout models (Matsui et al., 1996; Varfolomeev et al., 1998).”
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“Because homozygous TRX knockout is embryonic lethal in mice (35), it has been impossible to determine whether TRX is required to maintain vascular redox homeostasis during age-related hypertension or whether it contributes to the regulation of hypertension.”
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Thiol Redox Transitions by Thioredoxin and Thioredoxin-Binding Protein-2 in Cell Signaling
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“Thioredoxin-knockout in mice is lethal for the early development and morphogenesis of the mouse embryo (Matsui et al., 1996), whereas thioredoxin-transgenic mice are more resistant to oxidative stress with longer life spans, compared with wild-type mice (Mitsui et al., 2002).”
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BackgroundSelenoproteins in the Human Placenta: How Essential Is Selenium to a Healthy Start to Life?
Hogan, C., & Perkins, A. V. (2022) · Nutrients · doi:10.3390/nu14030628 · Cited by 57
“The thioredoxin system is not limited to oxidative stress regulation, playing a variety of roles in cells, including transcription, cell growth control, immune responses, virus infection and in the regulation of cell death [74,77].”
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The intricate role of selenium and selenoproteins in erythropoiesis
Liao, C., Carlson, B. A., Paulson, R. F., & Prabhu, K. S. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.04.578 · Cited by 55
Mouse Models of Oxidative Stress Indicate a Role for Modulating Healthy Aging
Hamilton, R. T. (2012) · Journal of Clinical & Experimental Pathology · doi:10.4172/2161-0681.s4-005 · Cited by 53
“Evidence also indicates that Prx1 interacts and stabilizes in the inactive state p66Shc protein [155] with similar mechanisms to that observed between Trx1 and ASK1.”
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“Homozygous mutants carrying a targeted disruption of the thioredoxin gene died shortly after implantation, suggesting that thioredoxin expression is essential for cell survival and early differentiation in the mouse embryo (23).”
Self-citationOka, S., Hirata, T., Suzuki, W., Naito, D., Chen, Y., Chin, A., Yaginuma, H., Saito, T., Nagarajan, N., Zhai, P., et al. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.807735 · Cited by 55
“Trx1 / mice were described previously (35).”
Self-citationRedox-Regulated Mechanisms in Asthma
Hoshino, T., Okamoto, M., Takei, S., Sakazaki, Y., Iwanaga, T., & Aizawa, H. (2008) · Antioxidants and Redox Signaling · doi:10.1089/ars.2007.1936 · Cited by 53
“When preimplanted embryos were placed in culture, the inner cell masses of the homozygous mutant embryos failed to proliferate (64).”
Oxidized thioredoxin-1 restrains the NLRP1 inflammasome
(2022) · doi:10.1126/sciimmunol.abm7200 · Cited by 53
“embryonically lethal in mice (34), and we thus generated myeloid lineage–specific Txn1-null mice by crossing mice with a floxed Txn1 allele with mice harboring Cre recombinase expression under the myeloid lineage–specific Lyz2 promoter.”
Selenium and thyroid autoimmunity
Negro, R. (2008) · Biologics · doi:10.2147/btt.s2746 · Cited by 50
“Knockout mouse model for Trx gene (Txn) are not vital and homozygous mutants for TrxR1 die shortly after implantation as a result of failure to proliferate, suggesting that TrxR is essential for early differentiation and morphogenesis (Matsui et al 1996; Jakupoglu et al 2005).”
Fujii, J., & Imai, H. (2014) · Spermatogenesis · doi:10.4161/21565562.2014.979108 · Cited by 50
“A conventional Trx is essential for proliferating cells and, hence, it is fatal to its null mutant mouse.(37) There are 3 testisspecific Trxs that are expressed in spermatids: Sptrx-1 (TXNDC2), Sptrx-2 (TXNDC3), and Sptrx-3 (TXNDC8).”
BackgroundRedox homeostasis and age‐related deficits in neuromuscular integrity and function
Sakellariou, G. K., Lightfoot, A. P., Earl, K. E., Stofanko, M., & McDonagh, B. (2017) · Journal of Cachexia Sarcopenia and Muscle · doi:10.1002/jcsm.12223 · Cited by 51
Thioredoxin Regulates Cell Cycle via the ERK1/2-Cyclin D1 Pathway
Mochizuki, M., Kwon, Y.-W., Yodoi, J., & Masutani, H. (2009) · Antioxidants and Redox Signaling · doi:10.1089/ars.2009.2623 · Cited by 50
“Based on previous reports (18, 21, 31, 33), we predicted that in vivo TRX knockdown by itself induces cell death.”
Self-citationCaenorhabditis elegans : What We Can and Cannot Learn from Aging Worms
Gruber, J., Chen, C.-B., Fong, S., Ng, L. F., Teo, E., & Halliwell, B. B. (2014) · Antioxidants and Redox Signaling · doi:10.1089/ars.2014.6210 · Cited by 46
“Loss of Trx-1 in mice causes early embryonic lethality, and these mutants die shortly after implantation (152).”
Reynoso, E., Liu, H., Li, L., Yuan, A. L., Chen, S., & Wang, Z. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.799353 · Cited by 51
“Trx1 is an essential gene and, therefore, cannot be successfully knocked out in cells (45).”
BackgroundChew, E., Lu, J., Bradshaw, T. D., & Holmgren, A. (2008) · The FASEB Journal · doi:10.1096/fj.07-101477 · Cited by 49
Thioredoxin expression in the human endometrium during the menstrual cycle
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Self-citationDivvela, S. S. K., Gallorini, M., Gellisch, M., Patel, G. D., Saso, L., & Brand‐Saberi, B. (2025) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2025.1521336 · Cited by 57
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Redox regulation, protein S-nitrosylation, and synapse loss in Alzheimer’s and related dementias
Oh, C.-K., Nakamura, T., Zhang, X., & Lipton, S. A. (2024) · Neuron · doi:10.1016/j.neuron.2024.10.013 · Cited by 52
Human Protein Atlas of redox systems — What can be learnt?
Dammeyer, P., & Arnér, E. S. J. (2010) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2010.07.004 · Cited by 47
Ko, F. C. F., & Chow, K. L. (2002) · Development · doi:10.1242/dev.129.5.1185 · Cited by 46
Auranofin is a potent suppressor of osteosarcoma metastasis
Topkas, E., Cai, N., Cumming, A., Hazar-Rethinam, M. H., Gannon, O. M., Burgess, M. L., Saunders, N. A., & Endo‐Munoz, L. (2015) · Oncotarget · doi:10.18632/oncotarget.5704 · Cited by 46
“Thioredoxin 1 (TRX1) [8], thioredoxin 2 (TRX2) [9], TXNRD1 [10] and TXNRD2 [11] genes are essential to cell viability since deletions of these genes are embryonic lethal in mice.”
BackgroundZhao, L., Feng, Y., Shi, A., et al. (2017) · Ultrasound in Medicine & Biology · doi:10.1016/j.ultrasmedbio.2017.04.020 · Cited by 46
Eschenlauer, S. C. P., & Page, A. P. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m210510200 · Cited by 46
Effect of acrolein and glutathione depleting agents on thioredoxin
Yang, X., Wu, X., Choi, Y. E., Kern, J. C., & Kehrer, J. P. (2004) · Toxicology · doi:10.1016/j.tox.2004.06.056 · Cited by 45
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“Recombinant human TBP-2 protein and polyclonal antihuman TBP-2 antibody IgG fraction were prepared as previously described.((26,30,31)) Full-length human TBP-2 cDNA was supplied by Dr Akira Nishiyama (Department of Biological Responses, Institute for Virus Research, Kyoto University, Kyoto, Japan).”
MethodSelf-citationProduction and secretion of thioredoxin from transformed human trophoblast cells
Trapani, G. D., Perkins, A. V., & Clarke, F. M. (1998) · Molecular Human Reproduction · doi:10.1093/molehr/4.4.369 · Cited by 46
“Furthermore, a recent mouse gene deletion study clearly demonstrated that the removal of the thioredoxin gene prevented embryo development and implantation (Matsui et al., 1996).”
Harnessing altered oxidative metabolism in cancer by augmented prooxidant therapy
Firczuk, M., Bajor, M., Graczyk‐Jarzynka, A., Fidyt, K., Góral, A., & Zagożdżon, R. (2019) · Cancer Letters · doi:10.1016/j.canlet.2019.11.037 · Cited by 45
Redox-regulated fate of neural stem progenitor cells
Prozorovski, T., Schneider, R., Berndt, C., Hartung, H., & Aktaş, O. (2015) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2015.01.022 · Cited by 45
The Role of NOX4 and TRX2 in Angiogenesis and Their Potential Cross-Talk
Chen, C., Li, L., Zhou, H. J., & Wang, M. (2017) · Antioxidants · doi:10.3390/antiox6020042 · Cited by 43
“Homozygous knockout of any isoform in mice can cause early embryonic lethality [80,81].”
BackgroundInteracting with Thioredoxin-1—Disease or No Disease?
Zschauer, T.-C., Matsushima, S., Altschmied, J., et al. (2012) · Antioxidants and Redox Signaling · doi:10.1089/ars.2012.4822 · Cited by 43
“Its essential role was demonstrated by genetic targeting leading to severe developmental disorders in the early mouse embryo resulting in embryonic lethality (31).”
Structure, Mechanism, and Inhibition of Aspergillus fumigatus Thioredoxin Reductase
Marshall, A. C., Kidd, S. E., Lamont-Friedrich, S. J., Arentz, G., Hoffmann, P., Coad, B. R., & Bruning, J. B. (2019) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.02281-18 · Cited by 42
Kaarteenaho–Wiik, R., & Kinnula, V. L. (2004) · Journal of Histochemistry & Cytochemistry · doi:10.1369/jhc.4a6291.2004 · Cited by 41
“In addition to MnSOD, recent knockout studies have emphasized the importance of -GCS and Trx for normal development (Matsui et al. 1996; Dalton et al. 2000).”
BackgroundSkjærven, K. H., Jakt, L. M., Dahl, J. A., Espe, M., Aanes, H., Hamre, K., & Fernandes, J. M. O. (2016) · Scientific Reports · doi:10.1038/srep34535 · Cited by 42
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“temporal pattern during vertebrate embryogenesis and genetic deletion experiments in mammals have emphatically demonstrated that selenoproteins are essential for embryonic survival [1–3].”
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Melatonin inhibits paraquat‐induced cell death in bovine preimplantation embryos
Pang, Y., Sun, Y., Sun, W., Du, W., Hao, H., Zhao, S., & Zhu, H. (2015) · Journal of Pineal Research · doi:10.1111/jpi.12297 · Cited by 40
“Trx is not only essential for early differentiation and morphogenesis in mouse embryos [60], but can improve the in vitro development of porcine embryos [61].”
BackgroundOxidative stress defense and repair systems of the ocular lens
Brennan, L. (2011) · Frontiers in Bioscience-Elite · doi:10.2741/365 · Cited by 42
“Early embryonic lethality results from knockout of either Trx 1 (146) or Trx 2 (147) and it has also been shown in mice that a haploinsufficiency (a single functional copy of a gene, where insufficient product is made) of Trx 2 results in the reduction of ATP production and increased ROS production (148).”
BackgroundROS, thiols and thiol-regulating systems in male gametogenesis
Conrad, M., Ingold, I., Buday, K., Kobayashi, S., & Angeli, J. P. F. (2014) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2014.10.020 · Cited by 39
“For instance, mice lacking Txn1 and Txn2 die at the blastocyst stage and mid-gestation [46,47], respectively, and mice null for the respective reductases, the selenoenzymes Txnrd1 and Txnrd2, produce lethal phenotypes during early embryogenesis and the fetal phase, respectively [48,49].”
BackgroundHomozygous mutation in TXNRD1 is associated with genetic generalized epilepsy
Kudin, A. P., Baron, G., Zsurka, G., Hampel, K. G., Elger, C. E., Grote, A., Weber, Y. G., Lerche, H., Thiele, H., Nürnberg, P., et al. (2017) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2017.02.040 · Cited by 39
“Txnrd1 is early embryonically lethal [21], while in cultured fibroblasts the enzyme was shown earlier to be essential only when grown in the absence of pyruvate and in high glucose and at low density [18].”
BackgroundHägg, D. A., Englund, M. C. O., Jernås, M., et al. (2005) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2005.06.034 · Cited by 39
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“The general importance of mammalian thioredoxins, the substrates of TrxR, is stressed by the fact that thioredoxin knockout in mice leads to early embryonic lethality [37].”
BackgroundMasutani, H., & Yodoi, J. (2002) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/s0076-6879(02)47027-9 · Cited by 40
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“The overall biological importance of these two proteins is evident in the early embryonic lethality of Trx- and TrxR-null mice (Matsui et al. 1996, Jakupoglu et al. 2005).”
Thioredoxin protects fetal type II epithelial cells from hyperoxia-induced injury
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“in vitro.(31,32) Exogenous addition of Trx can prevent oxidant-induced apoptosis in neuroblastoma cells.”
BackgroundGene disruption in mice: Models of development and disease
Shastry, B. S. (1998) · Molecular and Cellular Biochemistry · doi:10.1023/a:1006865210012 · Cited by 37
Environmental Stressors in Health and Disease
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“Our results raise the possibility that loss of TRX-1 function aggravates influenza virus-induced pneumonia, although complete TRX-1 deficiency results in early embryonic lethality (45).”
ResultSelf-citationRecent progress in research on molecular mechanisms of autophagy in the heart
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“…concentrations of H2O2 (Leyens, Knoops, & Donnay, 2004); Thioredoxin (TXN), a disulfide reductase that reduces ROS levels (Bing et al., 2003;Matsui et al., 1996); KEAP1 and NRF2, which are involved in the transcriptional activation of genes that increase the expression of antioxidant…”
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“The well characterized of these, Trx1, is critical for mammalian development (Matsui et al., 1996).”
BackgroundSTAT3-RXR-Nrf2 activates systemic redox and energy homeostasis upon steep decline in pO2 gradient
Paul, S., Gangwar, A., Bhargava, K., et al. (2017) · Redox Biology · doi:10.1016/j.redox.2017.10.013 · Cited by 36
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“Trx-deficient mice are embryonic lethal, whereas Trx-overexpressing transgenic mice are more resistant than are control mice to various inflammatory responses.(9,21) Physiologically, Trx is thought to exert a cytoprotective effect against oxidative stress by scavenging ROS, perhaps in conjunction with Prx.”
BackgroundSelenium Deficiency Abrogates Inflammation-Dependent Plasma Cell Tumors in Mice
Felix, K., Gerstmeier, S., Kyriakopoulos, A., Howard, O. M. Z., Dong, H., Eckhaus, M., BEHNE, D., Bornkamm, G. W., & Janz, S. (2004) · Cancer Research · doi:10.1158/0008-5472.can-03-2672 · Cited by 36
“TRX is a growth factor in tumor cells, and TR-null mice are not viable (79).”
BackgroundStavreus-Evers, A. C. (2002) · Molecular Human Reproduction · doi:10.1093/molehr/8.6.546 · Cited by 36
“Thus, it can be concluded that Trx is of major importance during pregnancy both at implantation (Clarke et al., 1991; Matsui et al., 1996 ) and also later in pregnancy (Sahlin et al., 1997a).”
BackgroundInfluentialThioredoxin System in Premature and Newborn Biology
Das, K. (2004) · Antioxidants and Redox Signaling · doi:10.1089/152308604771978480 · Cited by 39
“Attempts to generate knockout mice by targeted disruption of the Trx gene resulted in early embryonic lethality, demonstrating the importance of Trx in embryonic development (49).”
Conrad, M., Schick, J., & Angeli, J. P. F. (2013) · Neurochemistry International · doi:10.1016/j.neuint.2013.01.010 · Cited by 35
“Interestingly, the PD associated protein DJ-1 was shown to suppress bound ASK1 activation in response to H2O2, thereby preventing the dissociation of ASK1 from Trx1 in response to stressor.”
InfluentialManoharan, R., Seong, H., & Ha, H. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.05.020 · Cited by 36
“5 days of gestation, resulting in the unavailability of Trx-null mouse embryonic fibroblast (MEF) cells [35].”
BackgroundInterplay between cytosolic disulfide reductase systems and the Nrf2/Keap1 pathway
Schmidt, E. E. (2015) · Biochemical Society Transactions · doi:10.1042/bst20150021 · Cited by 35
Hsu, Y.-J., Lin, C.-W., Cho, S.-L., Yang, W.-S., Yang, C.-M., & Yang, C.-H. (2020) · Antioxidants · doi:10.3390/antiox9080712 · Cited by 37
“Trxs are essential for life, and Trx gene deficiency is embryonic lethal [24,25].”
BackgroundBachschmid, M. M., Xu, S., Maitland, K. A., Ho, Y., Cohen, R. A., & Matsui, R. (2010) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2010.07.005 · Cited by 34
“Unlike thioredoxin knockout mice, which are not viable [20], Glrx KO mice developwithout overt abnormalities [13].”
BackgroundKobayashi‐Miura, M., Shioji, K., Hoshino, Y., Masutani, H., Nakamura, H., & Yodoi, J. (2007) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01316.2006 · Cited by 35
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“The regulation of the thioredoxin system is believed to be key in differentiation and morphogenesis in embryonic tissue (Matsui et al., 1996) and can influence early embryo viability and maturation (Clarke, 1992).”
BackgroundRoman, M. G., Flores, L. C., Cunningham, G. M., Cheng, C., Dube, S., Allen, C., Remmen, H. V., Bai, Y., Hubbard, G. B., Saunders, T. L., et al. (2020) · Aging Pathobiology and Therapeutics · doi:10.31491/apt.2020.03.009 · Cited by 35
“Essential roles of Trx1 and Trx2 in mammals were further proven by the studies with knockout mice null for either Trx1 or Trx2, which are embryonically lethal [31,32].”
BackgroundHydroperoxide-Reducing Enzymes in the Regulation of Free-Radical Processes
Sharapov, M. G., Gudkov, S. V., & Lankin, V. Z. (2021) · Biochemistry (Moscow) · doi:10.1134/s0006297921100084 · Cited by 36
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“n trx1 / and trx2 / embryonic lethal [34]”
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“In fact, the lack of thioredoxin is lethal during embryonic life ( 18 ).”
BackgroundPeroxiredoxin Systems in Mycobacteria
Jaeger, T. (2007) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-1-4020-6051-9_9 · Cited by 34
“A selective inhibition of the pathogen’s Trxs therefore appears to be extremely difficult, but would be mandatory, since Trx is essential in mammals ( Matsui et al., 1996 ).”
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Kamimoto, Y., Sugiyama, T., Kihira, T., Zhang, L., 村林, 奈., Umekawa, T., Nagao, K., Ma, N., Toyoda, N., Yodoi, J., et al. (2010) · Diabetologia · doi:10.1007/s00125-010-1784-y · Cited by 35
“In this regard, it is interesting to note that homozygous mutant mouse embryos that lack the Trx gene die shortly after implantation [41], which corresponds to the stage when the TRX protein expression begins in WT embryos.”
BackgroundSelf-citationPositionally-dependent chondrogenesis induced by BMP4 is co-regulated by sox9 and msx2
Semba, I., Nonaka, K., Takahashi, I., Takahashi, K., Dashner, R., Shum, L., Nuckolls, G. H., & Slavkin, H. C. (2000) · Developmental Dynamics · doi:10.1002/(sici)1097-0177(200004)217:4 · Cited by 124
Immune regulatory and neuroprotective properties of preimplantation factor: From newborn to adult
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Redox-Inactive Peptide Disrupting Trx1–Ask1 Interaction for Selective Activation of Stress Signaling
Kekulandara, D. N., Nagi, S., Seo, H., Chow, C. S., & Ahn, Y. (2017) · Biochemistry · doi:10.1021/acs.biochem.7b01083 · Cited by 33
Tissue distribution of quiescin Q6/sulfhydryl oxidase (QSOX) in developing mouse
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“Thioredoxin and glutaredoxin expression is regulated during development (Kobayashi et al. 2000; Jurado et al. 2003) and thioredoxin knockout mouse embryo die early ( Matsui et al. 1996 ).”
BackgroundSelenium deficiency as a putative risk factor for osteoporosis
Ebert, R., & Jakob, F. J. (2007) · International Congress Series · doi:10.1016/j.ics.2006.08.001 · Cited by 33
Expression pattern of cytosolic glutathione peroxidase (cGPx) mRNA during mouse embryogenesis
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“Homozygous mutation of thioredoxin gene in mice caused embryonic death in the preimplantation stage (Matsui et al. 1996).”
BackgroundNakamura, T., Oh, C.-K., Zhang, X., Tannenbaum, S. R., & Lipton, S. A. (2021) · Antioxidants and Redox Signaling · doi:10.1089/ars.2021.0081 · Cited by 33
“Mice with homozygous knockout (KO) of Trx1 or Trx2 genes show early embryonic lethality, consistent with the notion that Trx activity is critical for cell survival (99).”
Possible physiological function of thioltransferase in cells
Xing, K., & Lou, M. F. (2003) · The FASEB Journal · doi:10.1096/fj.02-1164fje · Cited by 32
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Self-citationGene expression in the mouse preimplantation embryo
Stanton, J. L., Macgregor, A. B., & Green, D. P. L. (2003) · Reproduction · doi:10.1530/rep.0.1250457 · Cited by 32
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“Global Trx1þ/- mice were described previously.(5) Due to early death of Trx1cKO mice, echocardiographic measurements and collection of heart samples were conducted at 2–5 weeks of age.”
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Thioredoxin Overexpression in Transgenic Mice
Nakamura, H., Mitsui, A., & Yodoi, J. (2002) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/s0076-6879(02)47043-7 · Cited by 31
Self-citationMerwin, J. R. (2002) · Carcinogenesis · doi:10.1093/carcin/23.10.1609 · Cited by 31
“As previous studies have shown that deletion of a mouse thioredoxin gene or a selenocysteine tRNA gene results in early embryonic lethality (4, 27 ), it may be necessary to develop conditional null alleles in order to investigate the role of the thioredoxin system in mammalian growth, development, oncogenesis and tumo…”
BackgroundEvolutionarily Conserved Role of Thioredoxin Systems in Determining Longevity
AlOkda, A., & Raamsdonk, J. M. V. (2023) · Antioxidants · doi:10.3390/antiox12040944 · Cited by 31
The role of redox environment in neurogenic development
Ostrakhovitch, E. A., & Semenikhin, O. A. (2012) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2012.08.002 · Cited by 30
Reddy, P. G., Bhuyan, D. K., & Bhuyan, K. C. (1999) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1999.1691 · Cited by 30
Boehler, C. J., Raines, A. M., & Sunde, R. A. (2013) · PLoS ONE · doi:10.1371/journal.pone.0071525 · Cited by 30
Metadata
- Authors
- Matsui, M., Oshima, M., Oshima, H., Takaku, K., Maruyama, T., Yodoi, J., & Taketo, M. M.
- Affiliations
- Kyoto University (JP)
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 1996-08
- Volume
- 178
- Issue
- 1
- Pages
- 179-185
- ISSN
- 0012-1606 (ISSN-L)
- OpenAlex
- W1991387227
- Cited by
- 546
- References
- 0
- Citations by year
- 2026: 10 · 2025: 10 · 2024: 7 · 2023: 15 · 2022: 16 · 2021: 12 · 2020: 10 · 2019: 18 · 2018: 13 · 2017: 22 · 2016: 14 · 2015: 24 · 2014: 26 · 2013: 18 · 2012: 25
- FWCI
- 3.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Health Sciences › Medicine › Reproductive Medicine › Reproductive Biology and Fertility
- Keywords
- thioredoxin, targeted gene disruption, mouse embryo, early embryonic lethality, preimplantation embryo, inner cell mass, embryo resorption, gastrulation, embryonic morphogenesis, embryonic differentiation
- MeSH terms
- Animals, Blastocyst, Cell Division, Decidua, Female, Embryonic and Fetal Development, Genes, Homozygote, Organ Culture Techniques, Phenotype, Thioredoxins, Mice, Knockout, Gene Targeting, Mice
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