Technology ID
TAB-2411
Stat5a Knockout (Stat5atm1Mam) Mouse Model for Mammopoietic and Lactogenic Signaling Studies
E-Numbers
E-116-2012-0
Lead Inventor
Hennighausen, Lothar (NIDDK)
Applications
Therapeutics
Research Materials
Diagnostics
Development Status
Pre-clinical
Lead IC
NIDDK
ICs
NIDDK
Stat 5a Knockout: Stat5a deficiency results in the loss of prolactin-dependent mammary gland development and lactogenesis.
Prolactin induces mammary gland development and lactogenesis. Binding of Prolactin to its receptor leads to the phosphorylation and activation of STAT (signal transducers and activators of transcription) proteins. Two Stat proteins, Stat 5a and Stat5b, are expressed in mammary tissues during pregnancy. Stat5a null mice developed normally, and were indistinguishable from hemizygous and wild-type littermates in size, weight and fertility. Mammary lobulo-alveolar outgrowth during pregnancy was reduced and females failed to lactate after parturition. Stat5b, despite 96% similarity to Stat5a, could not compensate for the loss of Stat5a. Stat5a is the principal and obligate mediator of mammopoietic and lactogenic signaling.
Prolactin induces mammary gland development and lactogenesis. Binding of Prolactin to its receptor leads to the phosphorylation and activation of STAT (signal transducers and activators of transcription) proteins. Two Stat proteins, Stat 5a and Stat5b, are expressed in mammary tissues during pregnancy. Stat5a null mice developed normally, and were indistinguishable from hemizygous and wild-type littermates in size, weight and fertility. Mammary lobulo-alveolar outgrowth during pregnancy was reduced and females failed to lactate after parturition. Stat5b, despite 96% similarity to Stat5a, could not compensate for the loss of Stat5a. Stat5a is the principal and obligate mediator of mammopoietic and lactogenic signaling.
Commercial Applications
Mouse model to study mammopoietic and lactogenic signaling.
Licensing Contact: