Diverse categories of elements get excited about the apoptotic pathway. One set of mediators performing in apoptosis are asparate specific cysteine proteases or caspases. Sequential activation of caspase specific Hedgehog inhibitor cascades includes a crucial role in the execution phase of cell apoptosis. recently noted that inhibition of caspase mediated anoikis is important for FGF2 sustained tradition of hESCs and iPS cells. The T cell lymphoma 2 family, composed of 25 pro and anti apoptotic people, oversees a apoptotic cascade and keeps a between previous, dying cells and newly formed cells. When antiapoptotic Bcl 2 family members are overexpressed, the rate of pro and anti apoptotic Bcl 2 family members is damaged and apoptotic cell death may be eliminated. Mouse ES cells overexpressing Bcl 2 proliferate in serum free and feeder free conditions when supplemented with LIF, revealing that attenuation of apoptosis is crucial for ES cell survival and self renewal. An anti apoptotic protein of the Bcl 2 family, Bcl xL, includes all four Bcl 2 homology domains. Bcl 2 and Plastid Bcl xL are expressed in undifferentiated hESCs and specific EBs. To boost the efficiency of hESC growth and differentiation, we examined the protective function of Bcl xL in dissociation caused hESC death. Here, we demonstrated that activated caspase 3 apoptotic cells, as well as gene expression of other apoptotic associated genes, were dramatically increased when hESCs were dissociated in to individual cells. Ectopic expression of Bcl xL stopped hESCs from undergoing apoptosis following enzymatic dissociation into single cells, causing both an increase of hESC colonies and an increase of differentiation performance to create EBs. But, hESC self renewal HC-030031 was not changed by overexpression of Bcl xL. Our research demonstrated that Bcl xL overexpression not only lowered apoptotic caspase 3 cells, but also downregulated expert apoptotic TNF signaling mediators. In addition, Bcl xL regulated gene expression of adhesion molecules, indicating a development of attachment and cloning efficiency of individual hESCs. One limiting factor for hESC and iPS cell expansion is poor cell survival during subcultures. To verify that hESCs underwent apoptosis after enzymatic dissociation, we considered apoptotic attack at various time points after hESC dissociation in to single cells. Caspase 3 functions as a vital mediator of apoptosis in mammalian cells, and activation of caspase 3 is one of the penultimate steps in apoptotic cell death pathways. Specific antibodies were used by us for the subunit of cleaved caspase 3 to determine caspase 3 activation following enzymatic dissociation of hESCs. Flow cytometry has been used to quantify the apoptotic cells containing activated caspase 3.