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Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Nov 19, 2013

 

The image shows the structure of the binding interface being evolved.







WHO Child Growth Charts

 

 

 

New technique for designing drugs to treat serious illnesses

Researchers exploit the power of evolution to create designer proteins.

An international team of researchers led by the University of Leicester has "harnessed the power of evolution" to create a new drug for possible use against heart disease,and inflammation.

Researchers in the Department of Cardiovascular Sciences and Department of Biochemistry at the University of Leicester, UK, together with colleagues in Cambridge, UK, the Italian Foundation for Cancer Research Institute of Molecular Oncology, and Yale University School of Medicine in the USA, have employed a new technique to create protein-based drugs.


"This technique harnesses the power of evolution to engineer specific functions into a protein, such as the ability to neutralise a toxin in order to activate healing.

"This involves using a particular cell type to generate millions of different variations of one protein, selecting the variations that have improved properties, and then repeating the cycle until the protein has been changed to conform to the exact properties we want."

Nick Brindle, PhD, professor and lead researcher, University of Leicester, United Kingdom.


To show how the method works, the group took a protein normally found in the body and evolved it into a form that can block a molecule involved in blood vessel growth and inflammation.


This new protein, called a ligand-trap, is being developed for the potential therapeutic treatment of heart disease, inflammation and other illnesses.


Said Professor Brindle: "The idea that you can evolve proteins into forms that do what you want is not new, but it has been very difficult to do this for many of the complex proteins that we want to use as drugs or for other applications.

"This new approach promises to make engineering of such proteins not only possible but relatively easy. In addition to medicine, these specifically evolved 'designer proteins' have a wide range of applications in the chemical, pharmaceutical, and agricultural industries.

"This is a big step forward. We are hoping that, over the next five years or so, this new protein can be developed into a form that could be used to treat inflammation and other conditions."

The work, being published in the Journal of Biological Chemistry, was funded by the Biotechnology and Biological Sciences Research Council (BBSRC), MRC and the Wellcome Trust. The Leicester team collaborated principally with Dr Julian Sale at the MRC Laboratory of Molecular Biology in Cambridge, with additional input from Dr Hiroshi Arakawa, Italian Foundation for Cancer Research Institute of Molecular Oncology, Italy, and Dr Jean-Marie Buerstedde at Yale University School of Medicine.

Professor Brindle added: "We are really excited about getting this technique to work and are already using it to make other new molecules that we think will be useful to people. It was a real bonus for us to be able to evolve the ligand trap - as this trap targets a molecule involved in a whole range of health problems."

Significance
Background: The ligand angiopoietin2 contributes to vascular diseases.

Results: A new directed evolution method was used to create a specific angiopoietin2 binding protein from a non-specific angiopoietin receptor.

Conclusion: The receptor binding specificity can be switched with just three residue changes.

Significance: The new protein has therapeutic potential and the directed evolution method has advantages for evolving mammalian proteins.

Abstract
Tie2 is a receptor tyrosine kinase that is essential for the development and maintenance of blood vessels through binding the soluble ligands Angiopoietin 1 (Ang1) and 2 (Ang2). Ang1 is constitutively produced by perivascular cells and is protective of the adult vasculature. Ang2 plays an important role in blood vessel formation and is normally expressed during development. However, its re-expression in disease states, including cancer and sepsis, results in destabilization of blood vessels contributing to the pathology of these conditions. Ang2 is thus an attractive therapeutic target. Here we report the directed evolution of a ligand trap for Ang2 by harnessing the B cell somatic hypermutation machinery and coupling this to selectable cell surface display of a Tie2 ectodomain. Directed evolution produced an unexpected combination of mutations resulting in loss of Ang1 binding but maintenance of Ang2 binding. A soluble form of the evolved ectodomain binds Ang2 but not Ang1. Furthermore, the soluble evolved ectodomain blocks Ang2 effects on endothelial cells without interfering with Ang1 activity. Our study has created a novel Ang2 ligand trap and provided proof of concept for combining surface display and exogenous gene diversification in B cells for evolution of a non-immunoglobulin target.

Original press release: http://www2.le.ac.uk/offices/press/press-releases/2013/november/new-technique-for-developing-drugs-to-treat-serious-illnesses