Excerpts from Recent Articles from 2010

2011 Back Issues

zips, necklaces and mobile telephones - December 2011
I would hate to leave the house without the odd necklace hanging round my neck. But I happen to be fortunate. Millions of other people are not. That is because a lot of jewellery contains the silvery-white metal known as nickel, which can cause disagreeable skin conditions. If nickel were confined to jewellery, things would not be so bad but it is also frequently found in zips, coins and mobile telephones for instance. And who, in our society, can easily dispense with any one of these items? 65 million people in Europe suffer from nickel allergy; that is a large part of the population. Nickel ions are able to creep off a necklace or a coin – following sweat or rubbing for example – and sink through the first layers of skin where they will trigger off an immune response resulting in dermatitis. But why does it happen in some people and not in others? The answer seems to reside in a very small region of a protein known as the toll-like receptor 4, or TLR4, which has been shown to be at the heart of nickel allergy. (PDF version - 336K bytes)
UniProt cross references
Toll-like receptor 4, Homo sapiens, (Human) : O00206
a missing sense - November 2011
We are reminded regularly of how fragile life is and how easily the subtle balance of our molecular make-up can be shifted and cause devastating effects. Deafness is one. Deafness can be brought about by a number of incidents. It can occur following an illness or an accident for example. Or it can be congenital. Pendred Syndrome afflicts one out of two thousand human beings and is characterised not only by deafness in both ears but also – though not always – by a swelling in the thyroid gland, otherwise known as goitre. The symptoms of Pendred Syndrome have been known for over a century, but scientists are only just beginning to understand what it is that can leave a human-being deprived of a sense which is so vital. One of the culprits is known as Pendrin – a protein which acts as an ion transporter. (PDF version - 165K bytes)
UniProt cross references
Pendrin, Homo sapiens, (Human) : O43511
a balanced mind - October 2011
When I leave for work every morning, I know exactly where to get my train. This may sound quite absurd but just imagine, for one moment, that you had no memory. You would always be losing your keys. You would never remember where you had left your shoes. And you’d probably fall down the front doorstep daily because you had forgotten there was one. Thanks to our faculty for memorising things, life is far easier for us. We learn how to talk. We learn to avoid awkward situations. We even remember who our children are. On the molecular front, there is a lot going on. It all has to do with neurons and their ability to pass on messages and connect to one another. Unsurprisingly, many proteins are involved in the processes of learning and memory, and much research has been done on them in the past years. There is one protein, however, known as RGS14, which is a bit of a conundrum. Indeed, RGS14 seems to have the intriguing role of suppressing memory... (PDF version - 376K bytes)
UniProt cross references
Regulator of G protein signaling 14 (RGS14), Mus musculus, (Mouse) : P97492
Regulator of G protein signaling 14 (RGS14), Homo sapiens, (Human) : O43566
life's tremors - September 2011
Destruction is sometimes necessary for life to continue. It may sound paradoxical but examples are many. Our body shreds the food we eat to use the parts to feed itself. Certain cells commit suicide when they are of no use anymore. And damaged proteins within our cells are degraded and disposed of before they do any harm. Unsurprisingly, these are processes which involve multiple molecular interactions and are part of complex biochemical pathways – and when something goes wrong, our body is likely to feel the consequences. There is growing evidence that Parkinson’s disease (PD) may well be caused by the accumulation, in certain neurons, of damaged proteins which – under normal circumstances – would have been degraded. Whether it is the accumulation of non-degraded proteins or the subsequent modified turnover of specific proteins which are the cause of PD, no one knows. But scientists have discovered one particular protein, suitably baptised “Parkin”, which seems to be at the heart of the matter. (PDF version - 111K bytes)
UniProt cross references
E3 ubiquitin-protein ligase parkin, Homo sapiens (Human) : O60260
a queen's dinner - August 2011
Besides Dr Jekyll, humans cannot become something else after dinner. Bees can. Feed honeybee larvae some royal jelly, and they will grow into a larger, fertile and longer-lasting individual. It is no scoop. Scientists have known about it for over a century now. Nonetheless, it is a very thought-provoking notion for biologists – it means that a living being’s fate can be quite dramatically altered depending on what it feeds upon, very early on in development. The systems we are most acquainted with have a strong genetic component; give us a gene, with an environment, and that will make you into a heavy-built, tall, bald or curly-haired person. But here is some jelly that will shape a bee’s destiny. More specifically, there is a protein in the royal jelly that seems to be able to trigger off a series of metabolic processes in bee larvae, which will gradually turn them into queens. The protein has been baptized royalactin. (PDF version - 449K bytes)
UniProt cross references
Major royal jelly protein 1 (Royalactin), Apis mellifera (Honeybee) : O18330
tipping the mind - June 2011
Talk about the other side of the coin. There is growing evidence that creativity may well go hand in hand with psychosis, in particular schizophrenia. Intuitively, it does not seem so far-fetched a notion. Just think of Salvador Dali, for example. Or Peter Sellers. But mental illness has been around for as long as humans, so why does evolution bother to preserve it? Precisely because of the advantages of a creative mind. Researchers are not suggesting that someone suffering from a mental disorder is inevitably a potential artist. Or vice versa. At least not quite… But what they are slowly demonstrating is that there seems to be a genetic predisposition for creativity and psychosis. And that this predisposition has exactly the same origin for both traits. More specifically, a protein known as neuregulin-1 may have the capacity – given the environment – to tip a mind into mental illness or genius. (PDF version - 53K bytes)
UniProt cross references
Neuregulin-1, Homo sapiens (Human) : Q02297
do it yourself - May 2011
It can take ages to meet the right partner. So much so that plants lost their patience millions of years ago and thought up something else: the art of selfing. Many flowering plants are indeed capable of extensive in-breeding – by way of a rather subtle form of hermaphroditism – to ensure their spread and survival. The common mouse-ear cress, Arabidopsis thaliana, which has become the model plant for botanists, is revealing how many plants are able to perpetuate their species by letting their pollen fertilise their own pistil. Which prompts the question: how does any given plant species avoid self-fertilisation in the first place? The answer, or at least part of it, is: the S locus. The S locus carries two genes whose protein products – SCR and SRK – are directly involved in A.thaliana’s capacity to self-pollinate or not, and may well illustrate the pathway used by many other plants. (PDF version - 170K bytes)
UniProt cross references
Defensin-like protein A, SCRA, Arabidopsis thaliana (Mouse-ear cress) : P0CG07
S-receptor-like serine/threonine-protein kinase SRK, Arabidopsis thaliana (Mouse-ear cress) : B0F2A9
on the spur of a whim - March 2011
There are a number of biological molecules which are involved in a bewildering amount of activities. Serotonin is one. First thought to have the sole potential of contracting blood vessels, over the years serotonin has demonstrated that there is more to it than meets its chemistry. Besides its vasoconstrictor properties, it is also believed to be involved in instances as diverse as embryonic development, mood, appetite, nausea, sleep, body temperature, ageing, premature ejaculation, pain, anxiety, aggression, memory, cognition and migraines. And no doubt, as time goes by – as it inevitably does – yet more activities will be added to serotonin’s already impressive panoply. It is hardly surprising, then, that serotonin has been shown to play a part in psychiatric shortcomings such as obsessive compulsive disorder and impulsivity. But serotonin cannot do this by itself; it needs a receptor to which it can bind. A receptor known as the 5-HT receptor. (PDF version - 61K bytes)
UniProt cross references
5-hydroxytryptamine receptor 2B, Homo sapiens (Human) : P41595
our hollow architecture - February 2011
We get on with our day-to-day life largely unaware of the continuous battles that are being led within us. Indeed, it is thanks to unceasing cellular hostilities inside our bodies that we are able to get on with our lives as we do. Unwelcome entities such as viruses, but also tumours, would use our bodies as a playground – spreading havoc in their wake – were it not for a system that Mother Nature has offered every multicellular being, namely an immune system. In particular, natural killer cells and cytotoxic T lymphocytes are able to recognise infected cells in the body, into which they inject various molecules that ultimately destroy them. But how is the death sentence relayed? By way of pores. And these pores are formed by proteins known as perforins which assemble into large aggregates to form a barrel-shaped tunnel through which the poison flows from one cell to another. (PDF version - 85K bytes)
UniProt cross references
Perforin-1, Homo sapiens (Human) : P14222
Perforin-1, Mus musculus (Mouse) : P10820
the twisted way of things - January 2011
Imagine reading these words and not being able to pronounce them. Or reading them and not being able to grasp their meaning. These are just two of the drawbacks that many children - and adults - suffer from. In fact, we all know of someone who suffers from a reading disability, a common form of dyslexia. And that is because five to ten per cent of the population is afflicted by it. Because of its frequency, much progress has been made to try and understand why some children are simply not able to deal with words the way their classmates are, and yet they lack neither intelligence nor education. In the past years, it has become clear that dyslexia seems to have a hereditary component thus implying that a gene, or a collection of genes, could be at the heart of it. In the recent past, scientists have managed to track down at least one protein, with the appealing name of KIAA0319, which may well have a role in dyslexia and is involved in brain development. (PDF version - 86K bytes)
UniProt cross references
Dyslexia-associated protein KIAA0319, Homo sapiens (Human) : Q5VV43


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