Social mixing is one of the key objectives of the housing policy in OECD countries. The Low-Income Housing Tax Credit (LIHTC) program, the largest affordable housing construction program in the US since 1986, has recently set creating mixed-income communities as one of the standards. As a project-based program, LIHTC developments are likely to influence residential mobility; however, little is known about its empirical effects. This study investigated whether new LIHTC projects are effective at attracting heterogeneous income groups to LIHTC neighborhoods, thereby contributing to creating mixed-income communities. Using unique individual-level household movement data combined with origin–destination neighborhood characteristics, we developed zero-inflated negative binomial (ZINB) models to analyze the LIHTC’s impact on residential mobility patterns in Franklin County, Ohio, US, from 2011 to 2015. The results suggest that the LIHTC attracts low-income households while deterring higher-income families, and therefore the program is not proved to be effective at creating mixed-income neighborhoods.

Inwardly rectifying potassium channels, Kir2 in particular, are crucial in shaping the action potential and stabilizing the resting potential. However, little is known about the subcellular localization of the Kir2.1 channel, an important component of the background current, IK1, in cardiac myocytes. The present study was designed to determine whether Kir2.1 channels are localized to the caveolar plasma membrane and regulated by caveolin‐3. We found that about 40% (43.81±3.75%, n=3) of the cellular Kir2.1 was retained in the caveolin‐enriched fractions in the adult rat cardiomyocytes. In contrast, clathrin heavy‐chain was detected across a broad range of the gradient fractions. Cholesterol was shown to be enriched in the cavelin‐rich fractions. Co‐immunoprecipitation from cardiac myocytes indicated that Kir2.1 was associated with caveolin‐3. Expression of caveolin‐3 in HEK293T cells transfected with Kir2.1 significantly increased Kir2.1 level in the caveolin‐enriched fraction by 60% (63.26±8.33%, n=3). Further, immunofluorescent staining showed that a significant portion of Kir2.1 colocalized with caveolin‐3 in both transfected HEK293T cells and cardiomyoctes. In conclusion, we demonstrate that a significant portion of Kir2.1 channels targets to the caveolin‐enrich plasma membrane of rat cardiac myocytes, and the caveolae‐targeting of recombinant Kir2.1 channels is regulated by caveolin‐3.