p60TRP

still more to come here … in the meantime look for p60TRP under Systems Biology.

Posted in Molecular Biology / Genetics, Research Tagged with:

FAM72 (p17) expression in the brain

FAM72 (p17) expression in the hippocampus of the brain. Immunohistochemical analysis of a wild-type mouse brain revealed that p17 is expressed in the hippocampus (a = CA1 region; b = dentate gyrus; c = CA3 region) and cortex (d). Scale

Posted in Molecular Biology / Genetics, Research Tagged with:

pMANI & Neurodegenerative diseases

Still more data will be published here soon:   Characterizing the neurite outgrowth inhibitory effect of Mani. Mishra M, Lee S, Lin MK, Yamashita T, Heese K. FEBS Lett. 2012 Sep 21;586(19):3018-23.   The novel protein MANI modulates neurogenesis and

Posted in Molecular Biology / Genetics, Research Tagged with:

p48ZnF mouse model

Our transgenic neuronal p48ZnF bioluminescence mouse model allows the study of higher brain functions in vivo in living mice. Neuron-specific over-expression of p48ZnF in the mouse brain. Differential Response in Transgenic and Wild Type Mice Neurons to Glutamate Stimulation: Current

Posted in Research, Systems Biology

p60TRP mouse models

Our transgenic neuronal p60TRP bioluminescence mouse model allows in vivo analysis in living animals. Our transgenic p60TRP mice allow in vivo analysis in living mice to study memory & learning effects, as well as higher brain cognitive functions Neuron-specific over-expression

Posted in Research, Systems Biology

The protein FAM72 (p17) signalling pathways in cancer

Schematic hypothesis of p17-mediated tumorigenesis by influencing p53 signalling pathways. During tomorigenesis p17 expression gets probably at two different loci (FAM72A/B) out of control. Upon DNA damage PPM1D regulates UNG2 action and suppresses BER through the modulation of various targets

Posted in Molecular Biology / Genetics, Research Tagged with:

E3 ligases and FKBP14 are potential drug targets for AD therapy

E3 ligases and FKBP14 are potential drug targets for AD therapy. Increasing the activity of non-canonical E3 ligases by drugs or gene therapy could prevent Tau aggregation. CHIP has been suggested to target phosphorylated Tau for ubiquitination and subsequent degradation;

Posted in Molecular Biology / Genetics, Research Tagged with:

The proposed AD model that involves Tau phosphorylation, prion-like misfolded protein propagation, and the deregulation of UPS, HSP90, and FKBP co-chaperones

The proposed AD model that involves Tau phosphorylation, prion-like misfolded protein propagation, and the deregulation of UPS, HSP90, and FKBP co-chaperones. In AD, various physiological conditions are altered, including kinase over-expression or Aβ-induction increases in cellular kinase activities. As a

Posted in Molecular Biology / Genetics, Research Tagged with:

Predicted interactions between Tau protein, FKBP and CHIP in AD

Predicted interactions between Tau protein, FKBP and CHIP in AD. FKBP12 catalyzes the hyperphosphorylated Tau assembly into PHF. The fate of HSP90-bound hyperphosphorylated Tau is determined by the binding of the HSP90 co-chaperone molecule. The binding of an FKBP51 co-chaperone

Posted in Molecular Biology / Genetics, Research Tagged with:

The ubiquitin proteasome system and molecular chaperone deregulation in Alzheimer’s disease

The factors involved in the development of Alzheimer’s disease (AD) neuropathology. In the Tau-hypothesis, activation of cellular kinases may phosphorylate Tau, which subsequently causes Tau to lose its affinity to the microtubule system and thus forming aggregates. As an important

Posted in Molecular Biology / Genetics, Research Tagged with:

Categories