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FGFR2 knockout is an embryonic lethal mutation and blocks limb bud initiation.

FGFR3 knockout. Complete knockout of the FGFR3 gene, the gene in which missense mutants cause short statue achondroplasia, fails to restrain cartilage growth at the bone growth plate, allowing bones to elongate excessively but fail to ossify.

This molecular probe may serve as a companion tool to identify and stratify patient populations based on the prevalence of the target A₃ adenosine receptors.

Small molecule drugs, A₃AR-selective agonists, are currently in advanced clinical trials for the treatment of hepatocellular carcinoma, autoimmune inflammatory diseases, such as rheumatoid arthritis, psoriasis, and dry eye disease, and other conditions.

The five Muscarinic Acetylcholine (ACh) receptors are G-protein coupled receptors (M1R-M5R). M3 muscarinic ACh receptors are present in the central nervous system and the periphery.

Researchers at NIDDK have developed polyclonal antibodies against the G protein, Gbeta5. Gbeta5 is a unique and highly specialized G protein that exhibits much less homology than other Gbeta isoforms (~50%) and is preferentially expressed in brain and neuroendocrine tissue. It is expressed prominently in the neuronal cell membrane, as well as in the cytosol and nucleus. Although this distribution pattern suggests that Gbeta5 may shuttle information between classical G protein-signaling elements at the plasma membrane and the cell interior, its function in the brain is largely unknown.

Adenosine modulates many physiological processes by activating specific adenosine receptors. These adenosine receptors play a critical role in the regulation of cellular signaling and are broadly distributed throughout the body. Thus, the ability to modulate adenosine receptor-mediated signaling is an attractive therapeutic strategy for a broad range of diseases. This technology relates to a group of compounds that display high affinity and specificity for the A1 adenosine receptor subtype.

The NIH announces a novel method for fast, simple, and accurate detection of nucleic acids outside the modern laboratory. Nucleic acid testing is highly specific and often provides definitive identification of a disease or pathogen. Methods to detect nucleic acid sequences and identify a disease or pathogen are dominated by PCR, but applying PCR-based techniques in remote settings is challenging. Researchers at the NIH have developed a universal, colorimetric, nucleic acid-responsive diagnostic system that uses two short peptide nucleic acid (PNA) probes and does not rely on PCR.

Q490L point mutation was introduced into the rat M3 muscarinic receptor cDNA to confer persistent, constitutive (ligand-independent) activity. Expression of the M3 receptor mutant was placed under the control of a 650 bp fragment of the rat insulin promoter II (RIP II) to limit expression to the islet beta cell.

Researchers at NIH have developed islet beta cell M3 muscarinic acetylcholine receptor knockout mouse. The mice were generated by crossing floxed mouse M3 muscarinic acetylcholine receptor mice with mice in which Cre recombinase was controlled by the beta-cell specific rat insulin promoter (RIP-Cre mice).

Researchers at NIH have generated transgenic mice in which the M3 muscarinic receptor is overexpressed in pancreatic beta cells. This was done by placing the receptor gene under the control of the 650 bp rat insulin promoter II (RIP II). The resulting mice show a pronounced increase in glucose tolerance and enhanced plasma insulin levels. Strikingly, these mutant mice were resistant to diet-induced glucose intolerance and hyperglycemia.