Bcl-2

Bcl-2 (B-cell lymphoma 2), encoded in humans by the BCL2 gene, is the founding member of the Bcl-2 family of regulator proteins that regulate cell death (apoptosis), by either inducing (pro-apoptotic) or inhibiting (anti-apoptotic) apoptosis. Bcl-2 is specifically considered an important anti-apoptotic protein and is thus classified as an oncogene.

Bcl-2 derives its name from B-cell lymphoma 2, as it is the second member of a range of proteins initially described in chromosomal translocations involving chromosomes 14 and 18 in follicular lymphomas. Orthologs (such as Bcl2 in mice) have been identified in numerous mammals for which complete genome data are available.

Like BCL3, BCL5, BCL6, BCL7A, BCL9, and BCL10, it has clinical significance in lymphoma.

Isoforms

The two isoforms of Bcl-2, Isoform 1, also known as 1G5M, and Isoform 2, also known as 1G5O/1GJH, exhibit a similar fold. However, results in the ability of these isoforms to bind to the BAD and BAK proteins, as well as in the structural topology and electrostatic potential of the binding groove, suggest differences in antiapoptotic activity for the two isoforms

Boron trichloride

Boron trichloride is the inorganic compound with the formula BCl₃. This colorless gas is a valuable reagent in organic synthesis. It is highly reactive toward water.

Production and structure

Boron reacts with halogens to give the corresponding trihalides. Boron trichloride is, however, produced industrially by direct chlorination of boron oxide and carbon at 500 °C.

The carbothermic reaction is analogous to the Kroll process for the conversion of titanium dioxide to titanium tetrachloride. In the laboratory BF₃ reacted with AlCl₃ gives BCl₃ via halogen exchange. BCl₃ is a trigonal planar molecule like the other boron trihalides, and has a bond length of 175pm.

A degree of π-bonding has been proposed to explain the short B− Cl distance although there is some debate as to its extent. It does not dimerize, although NMR studies of mixtures of boron trihalides shows the presence of mixed halides. The absence of dimerisation contrasts with the tendencies of AlCl₃ and GaCl₃, which form dimers or polymers with 4 or 6 coordinate metal centres.

BCL9

B-cell CLL/lymphoma 9 protein is a protein that in humans is encoded by the BCL9 gene.

Function

BCL9, together with its paralogue gene BCL9L (BCL9 like or BCL9.2), have been extensively studied for their role as transcriptional beta-catenin cofactors, fundamental for the transcription of Wnt target genes.

BCL9 and BCL9L have been shown to take part in other tissue-specific molecular mechanisms, showing that their role in the Wnt signaling cascade is only one aspect of their mode of action.

Clinical significance

BCL9 is associated with B-cell acute lymphoblastic leukemia. It may be a target of translocation in B-cell malignancies with abnormalities of 1q21. The overexpression of BCL9 may be of pathogenic significance in B-cell malignancies.

BCL9 and BCL9L are potential clinical targets for human cancers; for instance, the gene expression changes that they promote is associated with a poor outcome in colorectal cancer.

Like BCL2, BCL3, BCL5, BCL6, BCL7A, and BCL10, it has clinical significance in lymphoma.

BCL3

B-cell lymphoma 3-encoded protein is a protein that in humans is encoded by the BCL3 gene.

This gene is a proto-oncogene candidate. It is identified by its translocation into the immunoglobulin alpha-locus in some cases of B-cell leukemia. The protein encoded by this gene contains seven ankyrin repeats, which are most closely related to those found in I kappa B proteins. This protein functions as a transcriptional coactivator that activates through its association with NF-kappa B homodimers. The expression of this gene can be induced by NF-kappa B, which forms a part of the autoregulatory loop that controls the nuclear residence of p50 NF-kappa B.

Like BCL2, BCL5, BCL6, BCL7A, BCL9, and BCL10, it has clinical significance in lymphoma.

Interactions

BCL3 has been shown to interact with:

References

Further reading

External links