Involved in many cell functions, including pre-mRNA splicing, the aryl hydrocarbon receptor (AHR) pathway, F-actin organization and protein ubiquitination. Plays a role in the dynamic organization of the actin skeleton as a stabilizer of actin filaments by association with F-actin through Kelch repeats (PubMed:12213805, PubMed:16317045). Protects cells from cell death induced by actin destabilization (PubMed:16952015). Functions as modifier of the AHR/Aryl hydrocarbon receptor pathway increasing the concentration of AHR available to activate transcription (By similarity). In addition, functions as a negative regulator of BCR(KLHL20) E3 ubiquitin ligase complex to prevent ubiquitin-mediated proteolysis of PML and DAPK1, two tumor suppressors (By similarity). Inhibits pre-mRNA splicing (in vitro) (By similarity). May play a role in cell cycle progression in the nucleus. Homodimer; through the BTB domain. Interacts with AHR/Aryl hydrocarbon receptor (By similarity). Associated with actin filaments. Not associated with actin filaments (PubMed:15684717). Ubiquitous expression. In the heart, the highest expression is detected in the ventricles and the lowest in the atria. Expressed in dendrites and spines in neurons. Barely detected in the heart at 15.5 dpc, but clearly expressed in newborn heart with increased amount up to 8 weeks of age. Decreased expression in various organs and cultured cell lines by doxorubicin treatment which may reduce mRNA stability. When the BTB domain is lacking, AHR signaling induction promoted by IVNS1ABP is massively increased; Thus, the BTB domain inhibits AHR signaling induced by IVNS1ABP. Mice develop normally with no gross abnormalities. However, they display marked sensitivity to doxorubicin cardiotoxicity with increased number of cardiomyocytes apoptosis. Analysis of hearts from knockout mice reveal vacuolization and edema of cardiomaycytes. Transgenic mice overexpressing Ivns1abp develop normally with no gross abnormalities up to 7-month old. However, they display a marked resistance to the cardiotoxic effect of doxorubicin which is an anti-neoplastic agent known to affect actin skeleton and an effective drug for cancer therapy with cardiotoxicity as side effect. Overexpression of Ivns1abp in the heart protect cardiomyocytes from apoptosis and improved survival rate after doxorubicin injection. Disorganized actin skeleton is observed in cells transfected with isoform 2 (Nd1-S), which lacks the six kelch repeats.