actin

that’s my baby right there, more than 5 years in my head and another 2 for it to come out and now is that im trying to teach myself how to get it out via comic books cause I thought it was the cheapest. i’ll put this shit out 5 years from now if that’s what it takes for it to come out how it looks in my head. actin like I got 10K$ like these white boys making potato salad crowdfunders. 400$ of my own went away in a week on this shit. dique “scam” shut yo fool ass up and wait.

anonymous asked:

HEY CAN U WRITE A BLURB ABOUT HELPING GRUMPY MICHAEL BE UNGRUMPY

YO that’d be so cute ok he’d be pissed abt something and even though he doesnt take things out on you, he’s still actin a lil sassy and so you’d have to bribe him with pizza and video games and blowjobs and cuddles where you tell him how much you love him and just how amazing you find him until he finally smiles and kisses your forehead and you ask, “so you’re not gonna be a grumpy pants anymore?” and he just sighs and laughs and responds with a sarcastic, “maybe!”

anonymous asked:

They all actin like they never got a dip bj before

The best kind tbh, all that sweet yellow tinged dip spit runnin down your balls

Actin filaments constructed into circular shapes using micropatterened glass coverslips etched with deep UV lithography.

Image by Anne-Cécile Reymann and Manuel Théry, iRTSV.

THIS WEEK’S QUESTION!

Every Sunday, a question will be asked about one of the images from this past week. Be the first to answer correctly, and your blog will be promoted on Monday’s image post and Biocanvas’s main site!

After being outside without adequate sun protection, you notice your skin begins to peel after a few days. You later learn that your exposed, peeling skin is actually undergoing apoptosis, the programmed death of cells.

What is the benefit of your cells “committing suicide” after being exposed to prolonged sunlight?

Answer: UV radiation from sunlight can damage cellular DNA beyond repair. These cells are then induced to undergo apoptosis to prevent them from becoming potentially cancerous.

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The Cell’s Muscles and BonesTorsten Wittmann

Cell movement begins with lamellipodia. A thin sheet of actin filaments (light purple) that stretches out to the cell’s periphery, lamellipodia generate pushing forces that drive the cell forward. Microtubules (cyan) can barely penetrate this actin network, but they direct cell motility in other ways, such as controlling cell adhesion and acting as the cell’s internal compass.

Bee brains offer insights into how human memories form

University of Queensland scientists have discovered that genes switch off as memories are being formed, allowing for new connections between nerve cells.

The discovery could eventually lead to a key for treating conditions such as autism and dementia.

Researchers studying honeybees during learning activities have shown that memory management in the bee brain is controlled by small genetic elements called microRNAs that help regulate gene expression.

Queensland Brain Institute researchers Professor Charles Claudianos and Dr Judith Reinhard have led an international team which has discovered that these microRNAs could directly target the key developmental gene ‘actin’, which controls the ability of nerve cells to connect with other nerve cells.

“We believe the brain selectively controls the wiring of memory through microRNAs that switch off key genes that shape, connect and signal between neurons,” Professor Claudianos said.

“The brain is constantly managing all of the sensory experiences we receive at any one time, and retains some of these as memories based on the relative importance or significance of the experience, such as food, danger and sex, to name some examples.

“We are now gaining an insight into how this occurs.

“By understanding how we can control nerve cell development with the technology used in our study, we may eventually help redress disorders such as dementia and autism.

“The current hypothesis in autism is that those brains are over-connected, so getting a grasp of understanding how to regulate neural circuitry could provide future methods of tackling these problems.

“The nervous system behind memory formation is fundamentally no different between a honeybee and a human, so by studying bees we identify the basic biological processes that help us understand humans.”

Dr Reinhard said the research provided a fundamental understanding of how neural circuits were built and consolidated to retain memories.

“Memory is a fundamental component of many mental health disorders, so understanding the basic science behind memories will give us greater insight into many disorders,” she said.

“Human illnesses and diseases such as muscular myopathies, neurodevelopmental disorders and susceptibility to infection are caused by DNA mutations that affect actin and actin-related biological processes.

“Molecules such as microRNAs are thought to have evolved to shape biological processes through controlling the expression genes that function in that process. A single microRNA can control many genes that function in the nervous system.”

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Synthetic Biology:  'Actin Out ’
Actin filaments Nucleated in Circle shapes on Glass Cover Slips 
Micropatterned Using Deep UV Lithography

Imaging by Anne-Cécile Reymann, Manuel Théry
Institut de Recherches en Technologies et Sciences pour le Vivant - Grenoble, France

When your hard drive fails, you order a new one online and then swap it out. Why can’t we do that for biological parts as well?  

Actin filaments (yellow) can be induced to polymerize by providing a pattern etched onto a glass surface.

Actin is the most abundant protein in most eukaryotic cells, and the protein most interactive with other proteins. It plays a key role in many cellular functions, from cell motility and the maintenance of cell shape and polarity to the regulation of transcription. [ X ]

IMAGES
Actin filaments are nucleated in circle shapes (20–40 µm microns in diameter) using micropatterning.  The location of actin nucleators is micropatterned onto a circle using deep UV lithography on a glass coverslip. Actin polymerization is then induced by applying actin monomers, profilin, and the Arp2/3 complex.

A dense and branched meshwork of filaments assemble on the circle (bright yellow) while non-branched filaments grow out of the circle and form parallel bundles.

7% of actin monomers are labelled with Alexa568, which allows the filaments to be imaged with classical epifluorescence microcopy at 40x.

Source: Cell

Gravity: It’s the law even for cells

Everybody knows that cells are microscopic, but why? Why aren’t cells bigger? The average animal cell is 10 microns across and the traditional explanation has been cells are the perfect size because if they were any bigger it would be difficult to get enough nutrients and energy to support them. Which is roughly where things stood until last year when Princeton bioengineers Marina Feric and Cliff Brangwynne published a paper in Nature Cell Biology describing their probing of cellular inner space, the cell nucleus, and their discovery that gravity could limit cell size: specifically the way actin’s mechanical properties are finely tuned to resist the force of gravity but also allow flexibility and rigidity of the cell nucleus to support life.

F-actin mesh in onion epidermal cell. False coloured for depth.

Needless to say, microscopy has progressed radically since Leeuwenhoek first observed his “animalcules” through lenses.

It is now possible to dissect cells into their various microscopic components, aiding not only in modeling and visualisation but also treatment and the advancement of research. In the image above, scientists used a technique called stochastic optical reconstruction microscopy (STORM) to peer deeper into a kidney cell. Objects of interest – in this case a protein called actin involved in cell movement – are tagged with fluorescent markers, which light up under laser light. This composite image is formed from 230,000 frames and is detailed enough to illuminate individual actin fibres, which are less than a millionth of a centimetre thick. Such high resolution can reveal the effects of a disease or a genetic fault in the finest detail - advancing research and treatment to a whole new level simply through the power of visualisation.

Credit: Ke Xu/Harvard University and BPoD.

Bovine Pulmonary Artery Endothelial Cell

Mouse monoclonal anti-α-tubulin antibodies were localized to the microtubules in this fixed bovine pulmonary artery endothelial cell (BPAEC) and subsequently visualized using goat anti-mouse IgG antibodies conjugated to Alexa Fluor® 350 dye (blue). Next, F-actin was labeled with phalloidin conjugated to Alexa Fluor® 594 dye (red). Finally, the cell was incubated with wheat germ agglutinin conjugated to Alexa Fluor® 488 (green) to stain components of the endosomal pathways. This superimposed and pseudocolored photomicrograph was acquired sequentially using bandpass filter sets appropriate for DAPI, the Texas Red® dye and fluorescein, respectively.

Photo courtesy of the Life Technologies Corporation.

Heart cells producing smooth muscle, fluorescence deconvolution micrograph. Fluorescent dyes have been used to highlight tissues, cellular structures and proteins: actin (green), cell nuclei (blue), smooth muscle (red). Actin is a contractile muscle protein, but here it is being produced by a heart cell to form a peripheral adhesion site. Adhesion sites are part of the way muscles and other tissues anchor themselves to the surrounding tissues.

[Figure 1: Fluorescence microscopy image showing the growth cone (indicated by an arrowhead) of an axon touching another axon. Protocadherin-17 (green) and a WAVE complex protein (magenta), accumulate at the contact site (indicated by an arrow)]

A protein shepherd helps coordinate brain development

During brain development, neurons extend projections called axons to connect with other neurons. Axons from groups of neurons with the same function tend to extend together, but the mechanisms involved in keeping the growing axons in contact for collective extension have been unclear. Masatoshi Takeichi, Shuichi Hayashi and colleagues from the RIKEN Center for Developmental Biology and RIKEN Quantitative Biology Center have now revealed that the protein protocadherin-17 (Pcdh17) plays a crucial role in this coordinated axon growth and correct development of the nervous system.

The protocadherin family of proteins is involved in regulating cell interactions and movement, and some of these proteins have been linked to brain disorders. Pcdh17 is expressed in the amygdala—small areas of the brain that regulate emotion and social behavior.

Takeichi, Hayashi and their colleagues found that when the gene that encodes Pcdh17 was deleted in mice, fewer axons extended from the amygdala, and those that did failed to follow the usual side-by-side path. Too much Pcdh17, however, caused axons from different groups to interact anomalously. By manipulating the structure of the protein, the researchers showed that Pcdh17 molecules in neighboring axons normally bind to each other to hold extending axons together.

The team also looked for other proteins that interact with Pcdh17 inside cells. This search identified members of the five-protein complex known as WAVE. This complex controls actin polymerization—a process in which the protein skeleton of the cell is extended to allow cell migration. The WAVE complex is normally localized to structures called lamellipodia, which are found at cell edges and are required for cell movement.

“On interacting with Pcdh17, the WAVE complex becomes localized to cell-to-cell contacts and converts these sites into motile structures,” explains Takeichi. This localization was observed only at axon-to-axon contacts (Fig. 1). “We hypothesize that the motility of growth cones at the leading ends of extending axons is enhanced by the Pcdh17–WAVE complex.”

The findings show that Pcdh17 plays a role in both holding groups of axons together as they grow, and in recruiting the cellular machinery required for extension.

“We discovered a mechanism by which axons extend together. A deficiency in this process may cause brain defects,” says Takeichi. “Some of the other protocadherin proteins, such as Pcdh19, have been linked to disorders such as epilepsy and mental retardation in humans. We are now analyzing the cellular and molecular backgrounds of such diseases using mouse models.”