Pharmacology Dictionary

Bcl-2: Bcl-2 (B-cell lymphoma-related gene) is major mammalian gene that is known to inhibit apoptosis.

Bax:  Bax is a bcl-2 homolog that forms with bcl-2 and acts to accelerate apoptosis.

Bcl-x: Bcl-x is a gene in the bcl-2 family that inhibits apoptosis after trophic factor deprivation in vitro.

ABL and BCR encoding genes are normally located on chromosomes 9 and 22, respectively. The ABL gene encodes a tyrosine kinase enzyme whose activity is tightly regulated. By the Philadelphia translocation, two fusion genes are generated: BCR-ABL on the Philadelphia chromosome (abbreviated chromosome 2Z) and ABL-BCR on the chromosome 9. The BCR-ABL gene encodes a protein with deregulated tyrosine kinase activity. The presence of this protein in the CML cells is strong evidence of its pathogenetic role. The efficacy in CML of a drug that inhibits the BCR-ABL tyrosine kinase has provided the final proof that the BCR-ABL oncoprotein is the unique cause of CML.

The discovery of the Philadelphia chromosome (in Philadelphia in 1960) led to the identification in chronic myeloid leukemia (CML) cells of the BCR-ABL fusion gene and its corresponding protein.

Bartter’s syndrome (antenatal Bartter syndrome, hyperprostaglandin E syndrome) is an autosomal-recessive electrolyte disorder, producing hypokalemia, metabolic alkalosis, hyper-reninism, and hyperaldosteronisms.

• It has now been recognized to be caused by mutations in at least three transport proteins responsible for NaCl absorption in the loop of Henle. Besides mutations in the Na+/K+/2Cl-cotransporter, Bartter’s syndrome can also be caused by mutations in the K+ channel that is present in the apical membrane of the ascending limb (ROMK or KIR1.1).
• This K channel is a K-recycling pathway and its operation is a prerequisite for NaCl absorption through NKCC2.
• Clinically, Bartter syndromes types I and II are indistinguishable. In contrast, a milder form of Bartter’s syndrome is caused by mutations in the basolateral chloride channel (ClC-Kb), an exit pathway for cellular Cl.

A receptor on nerve endings within a synapse that responds to the released neurotransmitter from that neuron. This then feeds back to the same neuron and negatively regulates the synthesis and release of that neurotransmitter.

Autophagy derived from latin words “self eating” is a normal regulated cell process where cytoplasmic materials are degraded through the lysosomal machinery and the contents reused by the cell.

During this process, organelles like mitochondria together with long-lived proteins are sequestred in a double-membrane vesicle delivered and degrade in lysosomes inside the cell.

Autophagy is activated in case of nutrient deprivation and plays a crucial role in the destruction of bacteria, viruses, and unnecessary proteins aggregates in cell.

Autacoids are literally ‘self-medicating agents’ that are liberated from or produced by cells in response to a stimulus. They differ from hormones in that they usually act locally after release, rather than reaching their target organ via the bloodstream.

Arrestins act as adaptor proteins that bind to phosphorylated G protein-coupled receptors (GPCR) and link the receptors to clathrin-coated pits. β-Arrestins are essential in the internalization of many GPCRs.

alpha-2  antiplasmin, a naturally occurring inhibitor of fibrinolysis, is a single chain glycoprotein that forms a stable, inactive complex within plasmin and thereby prevents plasmin’s activity.

Annexins form an evolutionary conserved family of Ca2+ and phospholipid binding proteins implicated in membrane trafficking and the regulation of Ca2+ currents across membranes.