The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Prostatic-like acid phosphatase in human endometrial glands and its cyclic activity.

Estrogen-induced autocrine and paracrine growth factors are thought to stimulate endometrial proliferation. However, the proliferation is arrested at an early secretory phase although the amount of growth factors and their receptors remains constant. These receptors are protein tyrosine kinases which cause activating receptor autophosphorylation and phosphorylation of signalling substances. One inhibitory mechanism is the reverse dephosphorylation by phosphatases hydrolysing phosphotyrosines. Previously, an acid phosphotyrosine phosphatase activity was found in endometrial secretory glands. The purpose of this study was to evaluate its characteristics. Catalytic and immunohistochemical techniques were applied on sections obtained from human endometrium and other tissues. Endometrial acid phosphatase hydrolysed phosphotyrosine, not only at acid, but also at neutral pH values. An alternative substrate was alpha-naphthyl phosphate or beta-glycerophosphate but not phosphoserine. Activities were inhibited by tartrate and fluoride but not by formaldehyde. These catalytic properties are identical only to those of prostatic acid phosphatase (PAP). A PAP-like nature was also proved by positive PAP immunohistochemistry. In conclusion, endometrial glands contain a phosphotyrosine phosphatase which is identical to PAP. Its activity is menstrual-cycle-dependent, being present only at the secretory phase, and it may counterbalance receptor tyrosine kinases terminating glandular proliferation despite constant levels of growth factors and their receptors.[1]


WikiGenes - Universities