Apeptide hormone rapidly inhibiting osteoclast activity. The relevance of calcitonin in human calcium homeostasis is not well understood. Calcitonin has been used for the treatment of osteoporosis, although due to the availability of more potent drugs with less side effects, and the lack of clear data on the anti-fracture efficacy of calcitonin, its clinical use has been steadily declining.

Calcium-dependent serine/threonine phosphatase (also known as protein phosphatase 2B or PP2B).

Calcineurin is a heterodimer composed of a catalytic subunit (Calcineurin A) and a regulatory subunit that contains an autoinhibitory domain (Calcineurin B). The catalytic subunit also contains a calmodulin-binding domain. Binding of calcium to the regulatory sununit allows the binding of calmodulin to the catalytic subunit, resulting in displacement of the autoinhibitory domain and enzymatic activation.

Calcineurin has many functions within eukaryote cells but is best known for its role in activating transcription of the interleukin 2 (IL-2) gene. IL-2 is required for activation of B- and T- cells and thus calcineruin inhibitors such as cyclosporin A and FK506, are potent immunosuppressants.

Cachexia refers to a physical wasting due to loss of muscle and fat.

Cachexia is often found in end-stage cancer patients but is also caused by autoimmune disorders or by infectious diseases such as AIDS and tuberculosis.

BDNF (brain-derived neurotrophic factor) is a neurotrophin, i.e. a target-derived growth factor, which is expressed in the brain predominantly in the hippocampus.

It acts through its tyrosine kinase receptor, trkB, which after ligand activation induces phosphorylation of intracellular signalling proteins on tyrosine residues.

BDNF expression is suppressed by stress hormones, and increased by antidepressants through a yet unknown mechanism.

The breast cancer resistance protein (BCRP) belongs to the G-branch of the ABC-transporter family (ABCG2). In contrast to most other ABC-proteins, BCRP consists of only one transmembrane domain (TDM) with one nucleotide binding fold (NBF) at its C-terminus.

Because of this structural characteristic BCRP as well as other ABC-transporters with only one TMD are termed half transporters.

To achieve functional activity these transporters have to form hetero- or homodimers.

BCRP is involved in the multidrug resistance of certain tumors and transports endogenous compounds like cholesterol and steroid hormones.

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.