We present the STM investigation of four different oligopyridines at the liquid/highly oriented pyrolytic graphite interface. The heteroaromatic compounds are constitutional isomers showing the same overall shape regardless of their actual conformation. On the basis of weak intermolecular C-H...N hydrogen-bonding interactions, different nanopatterns are formed following a simple general concept for the two dimensional self-assembly. The molecules arrange either in linear or in cyclic structures. Though the oligopyridines are achiral, the formation of prochiral trimeric superstructures leads to chiral phases due to the immobilization on the surface. Some of the molecules show polymorphic structures depending on the solvent. The large variety of the presented structures formed by self-assembly of the different oligopyridines which retain the same functional heteroaromatic backbone shall open the possibility of exploiting these patterns as templates for the nanostructuring of surfaces with guests such as small molecules or metal ions for intriguing applications in, for example, catalysis.

The transcriptional co-activator BOB.1/OBF.1 was originally identified in B cells and is constitutively expressed throughout B cell development. BOB.1/OBF.1 associates with the transcription factors Oct1 and Oct2, thereby enhancing octamer-dependent transcription. In contrast, in T cells, BOB.1/OBF.1 expression is inducible by treatment of cells with PMA/Ionomycin or by antigen receptor engagement, indicating a marked difference in the regulation of BOB.1/OBF.1 expression in B versus T cells. The molecular mechanisms underlying the differential expression of BOB.1/OBF.1 in T and B cells remain largely unknown. Therefore, the present study focuses on mechanisms controlling the transcriptional regulation of BOB.1/OBF.1 and Oct2 in T cells. We show that both calcineurin- and NF-κB-inhibitors efficiently attenuate the expression of BOB.1/OBF.1 and Oct2 in T cells. In silico analyses of the BOB.1/OBF.1 promoter revealed the presence of previously unappreciated combined NFAT/NF-κB sites. An array of genetic and biochemical analyses illustrates the involvement of the Ca2+/calmodulin-dependent phosphatase calcineurin as well as NFAT and NF-κB transcription factors in the transcriptional regulation of octamer-dependent transcription in T cells. Conclusively, impaired expression of BOB.1/OBF.1 and Oct2 and therefore a hampered octamer-dependent transcription may participate in T cell-mediated immunodeficiency caused by the deletion of NFAT or NF-κB transcription factors.

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The transcriptional co‐activator BOB.1/OBF.1 is crucial for Octamer‐driven transcription in B cells. BOB.1/OBF.1‐deficiency leads to tremendous defects in B‐cell development and function. Therefore, in the past research focused on the identification of BOB.1/OBF.1 target genes. However, the regulation of BOB.1/OBF.1 expression itself is poorly understood. Here we show that in B cells NF‐κB as well as to some extent NFAT proteins are involved in the activation of basal as well as inducible BOB.1/OBF.1 expression by direct binding to the BOB.1/OBF.1 promoter. Moreover, the analysis of different inducers of NF‐κB, like several TLR ligands, TNF‐α, BAFF, or LTα1β2, revealed that both the canonical and noncanonical NF‐κB pathways are involved in the induction of BOB.1/OBF.1 gene. The identification of so far unknown inducers that regulate BOB.1/OBF.1 expression in B cells provides novel insights in the potential function of BOB.1/OBF.1 during different aspects of B‐cell development and function.