MSK knockout mice still produce miR-132 in response to BDNF, but at a significantly lower level, indicating that there may be an alternative pathway operating.

[1] Activators of CREB phosphorylation, for instance forskolin and KSHV binding to endothelial cell targets, can also enhance miR-132 production in vitro.

[6] miR-132 has been found to associate with Fragile X Mental Retardation Protein FMRP, and may be involved in the selection of mRNAs, including those regulating synaptic function, to undergo translational suppression via an FMRP-dependent mechanism.

[8] Outside the brain, miR-132 can also modulate inflammation; transcription is stimulated by LPS and upregulated at a fairly early stage of herpesvirus infection.

In this instance, the target of translational suppression appears to be p300, a protein that associates with CREB and is an important mediator of antiviral immunity.

miR-132 is only transiently induced following infection; the silencing of p300 results in a reduction in CREB-mediated transcription from the miR-212/132 cluster, thus forming a negative feedback loop.

[9] Plasma from patients with rheumatoid arthritis (RA) has been found to contain lower levels of miR-132 compared to samples from healthy individuals.

This process is implicated in the chronic inflammation that may underlie insulin resistance in the obese, and may occur in response to serum deprivation.

Angiogenic factors such as VEGF and bFGF are CREB activators which could theoretically induce miR-132 production in endothelial cells.

[13] miR-132 also comprises part of the recently identified miRNA 'signature' of mammalian osteosarcoma, although a direct role in oncogenesis is yet to be fully described.