Disease relevance of Nab1

• Nab1 overexpression suppressed adrenergically induced and pressure overload-induced hypertrophy, whereas physiological growth during development and in response to exercise was not affected [1].
• The transcriptional repressor Nab1 is a specific regulator of pathological cardiac hypertrophy [1].

High impact information on Nab1

• Nab1 is highly expressed in mammalian cardiac myocytes and it inhibited cardiomyocyte hypertrophy through repression of its targets, transcription factor Egr [1].
• Mice lacking both Nab1 and Nab2 show severe congenital hypomyelination of peripheral nerves, with Schwann cell development arresting at the promyelinating stage, despite elevated Egr2 expression [2].
• Here we provide evidence that Nab1 and Nab2 proteins are critical transcriptional modulators of Egr2 in myelinating Schwann cells [2].
• Furthermore, misexpression of Nab1 or Nab2 in zebrafish embryos leads to alterations in the expression patterns of several hindbrain markers, consistent with an inhibition of Krox-20 activity [3].
• Finally, GnRH not only induced expression of Egr1, but also its corepressor, NGFI-A (Egr1) binding protein (Nab1), which can repress Egr1- induced transcription of the eLH beta promoter [4].

References