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The heart-failure relevant Potassium Channel Interacting Protein 2 (KChIP2) augments Ca V 1.2 and K V 4.3. KChIP3 represses Ca V 1.2 transcription in cardiomyocytes via interaction with regulatory DNA elements. Hence, we tested nuclear presence of KChIP2 and if KChIP2 translocates into the nucleus in a Ca 2+  dependent manner. Cardiac biopsies from human heart-failure patients and healthy donor controls showed that nuclear KChIP2 abundance was significantly increased in heart failure; however, this was secondary to a large variation of total KChIP2 content. Administration of ouabain did not increase KChIP2 content in nuclear protein fractions in anesthetized mice. KChIP2 was expressed in cell lines, and Ca 2+  ionophores were applied in a concentration- and time-dependent manner. The cell lines had KChIP2-immunoreactive protein in the nucleus in the absence of treatments to modulate intracellular Ca 2+  concentration. Neither increasing nor decreasing intracellular Ca 2+  concentrations caused translocation of KChIP2. Microarray analysis did not identify relief of transcriptional repression in murine KChIP2 −/−  heart samples. We conclude that although there is a baseline presence of KChIP2 in the nucleus both  in vivo  and  in vitro , KChIP2 does not directly regulate transcriptional activity. Moreover, the nuclear transport of KChIP2 is not dependent on Ca 2+ . Thus, KChIP2 does not function as a conventional transcription factor in the heart.

Potassium Channel Interacting Protein 2 (KChIP2) is not a transcriptional regulator of cardiac electrical remodeling