The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice. Xu also found that the mice with the same Bdnf mutation grew to be severely obese

large-scale genome-wide association studies showed Bdnf gene variants are, in fact, linked to obesity.

both leptin and insulin stimulate synthesis of BDNF in neuronal dendrites in order to move their chemical message from one neuron to another through synapses. The intent is to keep the leptin and insulin chemical signals moving along the neuronal highway to the correct brain locations, where the hormones will turn on a program that suppresses appetite.

"If there is a problem with the Bdnf gene, neurons can't talk to each other, and the leptin and insulin signals are ineffective, and appetite is not modified

One possible strategy would be to produce additional long-form Bdnf transcript using adeno-associated virus-based gene therapy, Xu says. But although this kind of gene therapy has proven to be safe, it is difficult to deliver across the brain blood barrier,

It’s assumed the protein complex is analyzing, but the mechanism of analysis is unknown. It’s also unknown if the UvrAB complex (or similar complex) actually does the repair, or if it signals for some other protein complex(es) to make the repair.

most protein reconfigurations occur in nanoseconds

In research on proteins, it was assumed (given their chemical composition) proteins would uniformly fold as they cool down and unfold as they heat up. (Think of a balloon expanding and shrinking with the temperature of the air inside.) The experiments didn’t bear this out; the rate of folding or unfolding according to temperature change was unequal (asymmetric) and uneven (nonlinear).

In recent biochemistry a great deal of work is done with ‘tagging’ or ‘marking’ molecules with fluorescent and phosphorescent materials. It’s well known that fluorescence and phosphorescence are phenomena closely related to protein folding and they can only be understood in terms of quantum transition between molecules.

With a quantum transition, the protein could change configuration by ‘jumping’ – skipping all the transition steps – to the final configuration. They call this quantum folding and they developed a mathematical model that shows how the folding, which is virtually instantaneous, would react to change in temperature.

Their quantum transition model matched the folding curves for 15 different proteins and also provides an explanation for the different rates of folding and unfolding among these proteins.

Luo and Lu’s paper is short, a mere 16 pdf pages, and the model is unpretentious mathematically. (Luo has several other related papers on arXiv.) It comes from unknown researchers in an unknown corner of the academic world, and it’s published on the open-source arXiv system. The lack of pedigree means that it will take more time than usual for scientists around the world to learn of it, examine it, and possibly test it.

Analysis of miR-375 levels in a human disease characterized by IL-13 overproduction - the allergic disorder eosinophilic esophagitis (EE) - revealed downregulation of miR-375 in EE patient samples compared with control patients. Low levels of miR-375 expression levels indicated disease activity.

“MiR-375 is proof of principle that microRNAs are involved in fine-tuning IL-13-mediated responses, which opens up a set of new possibilities for novel therapeutic targets for treatment of allergic disease.”

“The identification of a microRNA that regulates IL-13-induced changes and inflammatory pathways is a significant advancement for the understanding and future treatment of allergic disease,

Hoogsteen base pairs were known to exist primarily in RNA and had been observed in DNA only when there was damage to the DNA structure, or something else like a protein or drug was bound to it.

In RNA the Hoogsteen base pairs have been studied fairly extensively. They are considered an “excited state” and are useful to observe unusual protein binding. In DNA the Hoogsteen base pairing, which by the way has two forms, normal and reverse, was considered an anomaly.

It was discovered that normal DNA undergoes these shifts about 1% of the time and they last only milliseconds.

“Together, these data suggest that there are multiple layers of information stored in the genetic code.” Because critical interactions between DNA and proteins are thought to be directed by both the sequence of bases and the flexing of the DNA molecule, these excited states represent a whole new level of information contained in the genetic code.

The study defined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression--or output--of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited, and energy production was compromised, leading to stalled cell growth.

Geng Wang developed a strategy to target and import specific RNA molecules encoded in the nucleus into the mitochondria and, once there, to express proteins needed to repair mitochondrial gene mutations.

First, the researchers had to find a way to stabilize the reparative RNA so that it was moved out of the nucleus and then localized to the mitochondrial outer membrane. This was accomplished by modifying an export sequence to direct the RNA to the mitochondrion. Once the RNA was in the area of the transport machinery on the mitochondrial surface, then a second transport sequence was required to direct the RNA into the targeted organelle. With these two modifications, a wide range of RNAs were targeted to and imported into the mitochondria, where they worked to repair defects in mitochondrial respiration and energy production in two different cell line models of human mitochondrial disease.