gnaling system are not taken into account in the presented model, the model of the b1-adrenergic signaling system still describes reasonably well most of the available experimental data on mouse ventricular myocytes. The author considers this model as the first step in the development of a more comprehensive compartmentalized model of the adrenergic signaling system in mouse ventricular myocytes. Mammary gland development occurs predominantly after birth when the mammary gland anlage starts to invade the fat pad as a tree of growing and branching ducts. At this stage the end of the ducts exhibit teardrop shaped structures called terminal end buds, which disappear when the adult virgin gland has been fully developed. The duct epithelium consists of luminal and myoepithelial basal cells. TEBs contain as an outermost layer the cap cells and as 610 innermost layers the so called body cells. High proliferation and balanced apoptosis in the 
TEB compartment drive the development of the mammary gland ductal tree from puberty to the adult virgin state. During pregnancy, hormones like estrogen, progesterone or prolactin induce a further expansion of the duct tissue as well as the formation of alveoli which almost completely displace the adipose tissue of the fat pad. In late pregnancy the synthesis of milk proteins is initiated. After weaning, the glandular tissue involutes by apoptosis and autophagy, leading to a virgin-like structure of the mammary gland. The transcription factor Myc is important for the growth of tissues and organisms, either by controlling cell number or cell size and plays a pivotal role in a variety of cancers including breast cancer. During pregnancy the mammary gland undergoes dramatic changes including an increase of size. A conditional knockout of Myc in mammary gland epithelial cells PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19640586 during pregnancy delays the alveolar development by attenuation of cell proliferation and reduced milk production. In contrast, overexpression of Myc between D12.5 to D15.5 induces a precocious lobuloalveolar development and lactation, leading to a premature mammary gland involution. This accelerated mammary gland development during pregnancy is strongly correlated with an activation of Signal Transducer and Activator of Transcription 5 induced by down-regulation of the Stat5 inhibitor caveolin-1. Stat5, originally described as mammary gland factor , is a Pyrroloquinolinequinone disodium salt central regulator in mammary gland development, being mainly activated by Janus Kinase 2. Jak2 in PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19639654 turn integrates signals from different receptors like the growth hormone receptor, the estrogen receptor or the prolactin receptor, the latter being the most important one during pregnancy and lactation. Stat5 is expressed in the two homologous variants Stat5a and Stat5b, with Stat5a providing 70% of total Stat5 in the mammary gland. Recently, it was suggested that the particular functions during mammary gland development depend on the Stat5 concentration. Deletion of the largely redundant Stat5a/b variants during different stages of mouse mammary gland development prevents proper proliferation, differentiation and lobuloalveolar development during pregnancy and lactation. In contrast, ectopic expression of Stat5 in mammary gland epithelial cells induces alveolar fate commitment and lactogenesis. The transcription factor Miz1 contains 13 zinc finger motifs and a so called POZ domain at the N-terminus. Miz1 was originally identified as a Myc binding protein, forming a Miz1 in the Mammary Glan