LR1 has previously been shown to regulate c-myc transcription in B-cell lymphomas and Ncl has independently been found to be a c-myc target gene, were the c-Myc oncoprotein induces the levels of Ncl. Even more interesting is that LR1-binding activity was also reported to be dependent on Niltubacin inquirer phosphorylations of LR1 and our found interaction between Oct4 and Ncl is only occurring when Ncl is phosphorylated, indicating a similar mechanism for Ncl-P/Oct4 as components of a transcription factor complex in ES cells. All the above implies that Ncl-P is a component of a transcription factor complex together with Oct4 in ES cells. Although further investigations are required to verify this, by for example chromatin immunoprecipitation on sequences where Oct4 are known to bind, although none of our anti-Ncl works on immunoprecipitation so unfortunately we have not been able to perform the necessary experiments and can only speculate about it. Most interesting is the observed increase of Ncl-P/Oct4 complexes in spontaneously differentiated hESCs. It is tempting to speculate that Ncl-P works as a repressor to the activity of Oct4, by forming complexes with it when the ES cells start to differentiate. This might either allow transcription of genes repressed by Oct4 in ES cells or inhibit ES cell specific transcription. To conclude, we have identified two new interaction partners to Ncl in ES cells, both interactions occurring when Ncl is phosphorylated. Ncl-P/Tpt1 interact most prominently during mitosis and the interaction decreases upon retinoic acid induced differentiation; this indicates of a roll in cell proliferation or cell cycle regulation of rapidly dividing cells. Ncl-P/Oct4 interact in the nucleoplasm of interphase cells in both murine and human ES cells and show increased interaction in the beginning of spontaneously differentiated human ES cells. Similarities are found in the literature of Oct4 and Ncl binding sites as transcription factors, highly proposing Ncl-P to be together with Oct4 in a transcription factor complex in ES cells and that the complex formation is increasing during the initiation of spontaneous differentiation. Regarding our data here we propose Ncl-P as a connecting link between proliferation and transcription. Expression of Ncl-P may therefore improve reprogramming of somatic cells. Leukocyte adhesion deficiency 1 is an inherited disorder of neutrophil function characterized by recurrent bacterial infections and impaired pus formation and wound healing. The pathophysiology of LAD1 includes abnormalities of a wide variety of adhesion-dependent functions of hematopoietic cells due to deficiency of the beta-2 integrin subunit. Different types of mutations have been described in the CD18 gene.