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role of MTF-1 has been studied most extensively in the mouse. Besides coping with heavy metal load, MTF-1 can also mediate the induction of Mt genes in response to other stress situations, such as oxidative stress (5,17) and hypoxia (18). In addition, it is required for the metalloregulation of Znt1, encoding the major plasma membrane-localized zinc efflux transporter (19), the hypoxic/anoxic induction of the gene for placental growth factor (Plgf), an angiogenic protein of the vascular endothelial growth factor (VEGF) family (20), and has recently been invoked in tumor development (21,22). Furthermore, MTF-1 has an essential function during embryogenesis: targeted disruption of Mtf1 results in embryonic lethality around 14 days post coitum due to hepatocyte necrosis (23). In contrast, mice with null mutations for the stress-inducible metallothionein genes (Mt1 and Mt2) are viable, though sensitive to cadmium (24,25), indicating that additional important MTF-1 target genes are involved in the lethal phenotype. With the Cre-loxP conditional knockout technique, it is possible to circumvent the embryonic lethal phenotype of conventional Mtf1 knockout mice. Previous experiments with this technique revealed that deletion of Mtf1 from the liver after birth is no longer lethal under non-stress conditions (26)."}

{"project":"2_test","denotations":[{"id":"16221973-8824273-77403402","span":{"begin":219,"end":220},"obj":"8824273"},{"id":"16221973-10605938-77403403","span":{"begin":221,"end":223},"obj":"10605938"},{"id":"16221973-10096565-77403404","span":{"begin":238,"end":240},"obj":"10096565"},{"id":"16221973-10952993-77403405","span":{"begin":376,"end":378},"obj":"10952993"},{"id":"16221973-11289150-77403406","span":{"begin":537,"end":539},"obj":"11289150"},{"id":"16221973-15284217-77403407","span":{"begin":594,"end":596},"obj":"15284217"},{"id":"16221973-15516976-77403408","span":{"begin":597,"end":599},"obj":"15516976"},{"id":"16221973-9582278-77403409","span":{"begin":783,"end":785},"obj":"9582278"},{"id":"16221973-8367468-77403410","span":{"begin":928,"end":930},"obj":"8367468"},{"id":"16221973-8290567-77403411","span":{"begin":931,"end":933},"obj":"8290567"},{"id":"16221973-15226267-77403412","span":{"begin":1324,"end":1326},"obj":"15226267"}],"text":"The role of MTF-1 has been studied most extensively in the mouse. Besides coping with heavy metal load, MTF-1 can also mediate the induction of Mt genes in response to other stress situations, such as oxidative stress (5,17) and hypoxia (18). In addition, it is required for the metalloregulation of Znt1, encoding the major plasma membrane-localized zinc efflux transporter (19), the hypoxic/anoxic induction of the gene for placental growth factor (Plgf), an angiogenic protein of the vascular endothelial growth factor (VEGF) family (20), and has recently been invoked in tumor development (21,22). Furthermore, MTF-1 has an essential function during embryogenesis: targeted disruption of Mtf1 results in embryonic lethality around 14 days post coitum due to hepatocyte necrosis (23). In contrast, mice with null mutations for the stress-inducible metallothionein genes (Mt1 and Mt2) are viable, though sensitive to cadmium (24,25), indicating that additional important MTF-1 target genes are involved in the lethal phenotype. With the Cre-loxP conditional knockout technique, it is possible to circumvent the embryonic lethal phenotype of conventional Mtf1 knockout mice. Previous experiments with this technique revealed that deletion of Mtf1 from the liver after birth is no longer lethal under non-stress conditions (26)."}

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Besides coping with heavy metal load, MTF-1 can also mediate the induction of Mt genes in response to other stress situations, such as oxidative stress (5,17) and hypoxia (18). In addition, it is required for the metalloregulation of Znt1, encoding the major plasma membrane-localized zinc efflux transporter (19), the hypoxic/anoxic induction of the gene for placental growth factor (Plgf), an angiogenic protein of the vascular endothelial growth factor (VEGF) family (20), and has recently been invoked in tumor development (21,22). Furthermore, MTF-1 has an essential function during embryogenesis: targeted disruption of Mtf1 results in embryonic lethality around 14 days post coitum due to hepatocyte necrosis (23). In contrast, mice with null mutations for the stress-inducible metallothionein genes (Mt1 and Mt2) are viable, though sensitive to cadmium (24,25), indicating that additional important MTF-1 target genes are involved in the lethal phenotype. With the Cre-loxP conditional knockout technique, it is possible to circumvent the embryonic lethal phenotype of conventional Mtf1 knockout mice. Previous experiments with this technique revealed that deletion of Mtf1 from the liver after birth is no longer lethal under non-stress conditions (26)."}