In conclusion, we developed a new method for identifying immune cells based on a MALDI-TOF MS approach. A major advantage of this method compared to the usual techniques is the lack of purification steps and staining procedures, which often lead to cell activation. The cell database we constructed was useful for identifying a cell type within a cell mixture, and it could potentially be used to identify different functional states of a cell population such as monocytes or macrophages. Nuclear reprogramming of somatic cells is a promising route in cell replacement therapy that can be used to replace or restore normal function of damaged cells. The ultimate approach is to reprogram the patient’s own cell, which would avoid immunosuppression. The molecular mechanisms of nuclear reprogramming are still unsolved although recent reports have shown that reprogramming of human somatic cells can be achieved in vitro by retroviral expression of four transcription factors creating induced pluripotent stem cells, which are comparable to ES cells. One factor has been proven essential for successful iPS cell creation i.e. Oct4, which is an established ES cell and potent nuclear reprogramming factor. Successful reprogramming of somatic cells requires proper embryonic genome activation. In rhesus monkey, the major embryonic genome activation is thought to occur between the six- and eight-cell stages, which coincide with the timing of nucleogenesis. The nucleolus may therefore serve as a marker for embryonic genome activation. Nucleolin, one of the most abundant non-ribosomal proteins in the nucleoli, is a multifunctional protein, which belongs to a large family of RNA binding proteins and is a substrate to several kinases. Extensive phosphorylation occurs during interphase on serine residues by CK2, while cdc2 phosphorylate threonine residues during mitosis, and these phosphorylation patterns regulate Ncl functions and localization during the cell cycle. Ncl is functionally hyperactive in rapidly dividing cells compared to nondividing cells, and high levels of Ncl are found in tumors and other rapidly dividing cells such as ES cells, indicating several important functions during cell proliferation. A unique regulatory mechanism for Ncl expression has been revealed; Ncl has GDC-0199 increased stability in proliferating cells by inhibiting its self-cleaving activity. Down-regulation experiments using RNA-interference has proven that Ncl is essential for cell division, given that absence of Ncl results in prolonged cell cycle with misaligned chromosomes, defects in spindle organization, growth arrest and increased apoptosis. Ncl has also been reported to have a cell cycle-controlled interaction with the prototypical tumor suppressor Retinoblastoma protein.