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A nuclear-encoded factor implicated in coordination of photosystem II assembly and psbA messenger RNA biological translation.[ref]
Antizyme is a regulatory protein that binds ornithine decarboxylase, inhibits its activity and promotes its degradation. This limits a key entry step in polyamine synthesis. Production of antizyme itself can respond to polyamine availability through regulated biological translation, creating feedback between a metabolic product and the lifetime of its biosynthetic enzyme. The inhibitory protein is therefore part of a pathway-control system rather than an additional substrate of the decarboxylase reaction. [ref]
UniProtKB by the UniProt Consortium. P54368, Function, Catalytic activity and Subunit structure
A regulatory protein whose association with a cyclin-dependent kinase influences kinase activity and substrate control during the cell cycle.
An inhibitory regulator of separase. Its regulated destruction helps permit sister-chromatid separation.
Destruction is controlled by the anaphase-promoting complex, linking the cell-cycle decision to activation of the protease that removes a cohesion barrier. This makes protein turnover part of a switch that permits physical chromosome separation. [ref]
Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. Chapters 3, 6 and 15, protein function, translation and cell signalling
A guanine-nucleotide exchange factor involved in local activation of RhoA during animal cytokinesis.
Spatially restricted RhoA activation helps organize the contractile machinery at the cleavage site. The exchange factor therefore links positional information from the division apparatus to local cytoskeletal force generation. [ref]
Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. Chapters 3, 6 and 15, protein function, translation and cell signalling
A small GTPase that promotes actin assembly and myosin regulation during contractile-ring formation and other cellular processes.
A membrane-remodelling protein system involved in processes including the final membrane constriction and separation of animal cytokinesis.
A eukaryotic single-stranded DNA-binding complex participating in replication, repair and signalling responses.
Binding protects exposed single-stranded DNA and helps recruit other factors. Its presence can reflect normal replication or a response to damaged or stalled DNA structures, so it is not a unique marker of one pathway. [ref]
Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. Chapters 3, 6 and 15, protein function, translation and cell signalling
An intermediate-filament protein often used as one mesenchymal-associated marker. Its expression alone is not a complete definition of epithelial–mesenchymal transition.
Directed evolution iterates sequence diversification, functional screening or selection, and recovery of successful variants. A reliable genotype–phenotype link and an assay faithful to the desired property are more important than library size alone.
Rational protein design proposes sequences or substitutions using structural, chemical or evolutionary information. A plausible model narrows the search but does not establish that the resulting protein folds, binds or catalyses as intended.
Pinned article: Introduction to the OurBigBook Project
Welcome to the OurBigBook Project! Our goal is to create the perfect publishing platform for STEM subjects, and get university-level students to write the best free STEM tutorials ever.
Everyone is welcome to create an account and play with the site: ourbigbook.com/go/register. We belive that students themselves can write amazing tutorials, but teachers are welcome too. You can write about anything you want, it doesn't have to be STEM or even educational. Silly test content is very welcome and you won't be penalized in any way. Just keep it legal!
Intro to OurBigBook
. Source. We have two killer features:
- topics: topics group articles by different users with the same title, e.g. here is the topic for the "Fundamental Theorem of Calculus" ourbigbook.com/go/topic/fundamental-theorem-of-calculusArticles of different users are sorted by upvote within each article page. This feature is a bit like:
- a Wikipedia where each user can have their own version of each article
- a Q&A website like Stack Overflow, where multiple people can give their views on a given topic, and the best ones are sorted by upvote. Except you don't need to wait for someone to ask first, and any topic goes, no matter how narrow or broad
This feature makes it possible for readers to find better explanations of any topic created by other writers. And it allows writers to create an explanation in a place that readers might actually find it.Figure 1. Screenshot of the "Derivative" topic page. View it live at: ourbigbook.com/go/topic/derivativeVideo 2. OurBigBook Web topics demo. Source. - local editing: you can store all your personal knowledge base content locally in a plaintext markup format that can be edited locally and published either:This way you can be sure that even if OurBigBook.com were to go down one day (which we have no plans to do as it is quite cheap to host!), your content will still be perfectly readable as a static site.
- to OurBigBook.com to get awesome multi-user features like topics and likes
- as HTML files to a static website, which you can host yourself for free on many external providers like GitHub Pages, and remain in full control
Figure 2. You can publish local OurBigBook lightweight markup files to either OurBigBook.com or as a static website.Figure 3. Visual Studio Code extension installation.Figure 5. . You can also edit articles on the Web editor without installing anything locally. Video 3. Edit locally and publish demo. Source. This shows editing OurBigBook Markup and publishing it using the Visual Studio Code extension. - Infinitely deep tables of contents:
All our software is open source and hosted at: github.com/ourbigbook/ourbigbook
Further documentation can be found at: docs.ourbigbook.com
Feel free to reach our to us for any help or suggestions: docs.ourbigbook.com/#contact





