Analysis of structure and function of the gene FAM72

FAM72A­Zn2+ and RSM interactions. A) Zn2+-binding sites are shown on the developed 3D FAM72A protein structure. Suggested Zn2+-binding sites on the FAM72A protein are Csy18, Cys21, Cys74, and Cys77. B) The RSM ((2s)-2-(acetylamino)-Nmethyl-4-[(R)-methylsulfinyl] butanamide)-binding sites are shown on the developed

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In-place Merging Algorithm Benchmarking Tool

Below you can download a small Visual C++ project for benchmarking in-place merging algorithms.Some Notes: The zip file contains a Visual C++ 2008 project. However, the C++ code should be easily portable to other platforms/compilers as e.g. gcc. I created this

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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

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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

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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

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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;

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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

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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

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

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

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