http://www.cellbiolint.org/ Cell Biology International RSS feed -- Immediate Publications 1065-6995 1065-6995 Cell Biology International http://www.cellbiolint.org/images/cbi_mast_logo2.gif http://www.cellbiolint.org/ http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110662 in vitro and xenograft tumor growth in BALB/c nude mice in vivo were detected after NS knockdown. Results showed that PSMAp/e can drive EGFP silencing in LNCaP, not in PC-3, EJ and HEK293 cells and PSMAe/p-poly(A) combination achieved the best silencing efficacy. Then PSMAe/p-shNS-poly(A) drives NS knockdown in LNCaP cells, not in PC-3, EJ and HEK293 cells. Furthermore, RNAi-mediated NS knockdown not only reduces cell proliferation rate, reduces the percentage of S-stage cells and increases the percentage of G1-stage cells and increases the early apoptosis ratio in LNCaP cells in vitro, but also inhibited the LNCaP xenograft tumor growth in BALB/c nude mice in vivo by intratumoral injection. In conclusion, Our study demonstrated that PSMAe/p-poly(A) combination is a promising delivery system for targeted RNAi gene therapy of prostate cancer. We showed one effective antitumor strategy by targeting NS protein, an important target in prostate cancer, with PSMAe/p-shNS-poly(A). These results serve as an important step for developing novel strategies to treat prostate cancer.]]> R Liu, J Sun, Z Zhang, Y Xu 2012-05-21T13:46:17Z doi:10.1042/CBI20110662 Portland Press Limited 2012-05-21 Cancer http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110653 Tir mice provide an excellent study model for analyzing the sexual development process that occurs during gonadal differentiation; however the molecular mechanisms which contribute to sexual reversal are not clear. The aim of this study was to establish which molecular events may participate in the sexual reversal of the B6.Y^Tir mouse. The pattern of gene expression related to testicular (Sry, Sox9 and Mis) and ovarian (Wnt4, Rspo1 and Stra8) differentiation was studied, by applying immunofluorescence and real time RT-PCR and focusing on XY gonads from the B6.Y^Tir mouse, but also analyzing the normal strains CD-1 and C57/BL6J (B6). It was evident that the expression of genes related to the process of sexual differentiation is altered in the case of the B6.Y^Tir strain, both at the transcript and protein level inducing differentiation of ovaries and ovotestes; but not the formation of normal testicles. Our results indicated that the expression of testicular genes was inhibited at various levels, permitting the expression of ovarian genes such as Wnt4, Stra8 and Rspo1. However the activity of these genes was not clear when we analyzed our data as an average. Here we present a co-relation analysis indicating that an ovary differentiation pathway is activated, when the testicular differentiation pathway is inhibited.]]> N Rocio Antonio-Rubio, N Moreno-Mendoza 2012-05-14T14:18:58Z doi:10.1042/CBI20110653 Portland Press Limited 2012-05-14 Differentiation http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20120054 C Lv, Y Jiang, H Wang, B Chen 2012-05-14T14:16:52Z doi:10.1042/CBI20120054 Portland Press Limited 2012-05-14 Differentiation http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110687 in vitro model of the ovarian cancer cell line SKOV3 for the cell dispersal study. LPA induces rapid AJ disruption by increasing the internalization of N-cadherin-b-catenin. By using immunoprecipitations, we demonstrate that LPA induces increased tyrosine phosphorylation of b-catenin and alters the balance of b-catenin-bound SFK and phosphotyrosine phosphatase 1B (PTP1B). The altered balance of tyrosine kinase/phosphatase is correlated with a concomitant disintegration of the b-catenin-a-catenin, but not the b-catenin-N-cadherin complex. This disintegration of b-catenin from a-catenin and the cell dispersal caused by LPA can be further rescued by the blockage of SFK activity with the chemical inhibitor PP2. More importantly, PP2 also restores the level of PTP1B bound to b-catenin. We propose that LPA signaling alters AJ stability by changing the dynamics of tyrosine kinase/phosphatase bound to AJ proteins. Our study provides further understanding of the early signaling events regulating ovarian cancer cell dispersal and AJ disruption induced by LPA.]]> R Yun-Ju Huang, C Wen, C Liao, S Wang, L Chou, J Wu 2012-05-14T14:14:50Z doi:10.1042/CBI20110687 Portland Press Limited 2012-05-14 Cancer http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20100920 P value < 0.05 and absolute fold change < 2. These genes involved in many kinds of biological functions, including immune response, transcription regulation and metabolism process. 10 genes (IL8, GOS2, CXCR4, FOS, RPS24, HAP90AA1, PFDN5, RPL27, GZMA and PFN1) which showed significant difference were validated by Real-time PCR in 54 hepatocellular carcinoma patients and 56 healthy normal controls. 7 genes (IL8, GOS2, CXCR4, FOS, RPS24, HSP90AA1, PFN1) showed significant difference both Real time PCR and Microarray. The protein expression of IL8 and FOS were up-regulated in hepatocellular carcinoma when compared to the healthy control. We have identified the genes signature in peripheral blood which may classify the hepatocellular carcinoma patients and healthy controls.]]> P Zhang, R Wei, X Wen, L Ping, C Wang, Z Dong, X Deng, W Bo, C Bin, Y Tian 2012-05-14T13:22:30Z doi:10.1042/CBI20100920 Portland Press Limited 2012-05-14 Cancer http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20120060 P C Baer, J Bereiter-Hahn 2012-05-14T13:09:37Z doi:10.1042/CBI20120060 Portland Press Limited 2012-05-14 Differentiation http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110633 G Jiang, Y Zou, X Wu 2012-05-11T14:19:18Z doi:10.1042/CBI20110633 Portland Press Limited 2012-05-11 Cancer http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110586 E. coli for their binding and internalization. Previous studies in our laboratory have shown that nitric oxide (NO) can reduce the invasion of Dr (+) E. coli and the severity of uterine infection in pregnant rats. Also, the expression level of DAF both at the mRNA and protein levels has been shown to be reduced by NO. Therefore NO mediated down regulation of DAF appears to be an important factor in reducing the susceptibility to E. coli infection. However, it is unclear if NO can actually modulate the membrane association of DAF and therefore initial bacterial binding to cells. Here we show that NO induces the delocalization of DAF from the GM1 rich lipid rafts. Using biochemical and cell biological approaches in a uterine epithelial cell model (Ishikawa cells) we show that upon exposure to NO, DAF accumulates in caveolae. We also show that interaction of DAF with the caveolar protein, caveolin1 leads to their internalization in to endosomes. The NO induced delocalization of DAF from the lipid raft and its accumulation in caveolae are mediated through a cGMP pathway. The acute localized synthesis of NO and its influence on DAF localization may represent an important unrecognized phenomenon of host defense against Dr (+) E. coli bacteria, as well as many disease conditions that involve complement system.]]> M Banadakoppa, P Goluszko, D Liebenthal, C Yallampalli 2012-05-11T11:19:17Z doi:10.1042/CBI20110586 Portland Press Limited 2012-05-11 Trafficking http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110404 in vivo. Here, we propose that miR-15a and miR-16-1 may target cyclin B1 (CCNB1) which associates with several tumorigenic features such as survival and proliferation. The levels of miR-15a and miR-16-1 in colon cancer cells are inversely correlated with CCNB1 expression, and we found consensus between miR-15a/16-1 and CCNB1 mRNA sequences by analyzing homology. In the present study, vector-based miR-15a/16-1 expression plasmid was constructed and transfected into HCT 116 and SW620 colon cancer cells in vitro. The negative effects produced on cell viability and angiogenesis were analyzed using flow cytometric analysis, colony formation analysis and tube formation analysis. CCNB1 expression down-regulated was certified by western blotting analysis. Systemic delivery of miR-15a/16-1 plasmids encapsulated in cationic liposome led to a significant inhibition of subcutaneous tumor growth and angiogenesis in tumor tissues, whereas no effects were observed with liposome carrying the non-specific plasmid. Summarily, it’s the first time miR-15a/16-1 was applied into colon cancer treatment in vivo, and had resulted in colon tumor xenografts growth arrest and angiogenesis decrease effectively. These findings suggested that systemic delivery of vector-based miR-15a/16-1 expression plasmid might be a potential approach for human colon cancer therapy.]]> L Dai, W Wang, S Zhang, Q Jiang, R Wang, L Dai, L Cheng, Y Yang, Y Wei, H Deng 2012-05-11T11:09:26Z doi:10.1042/CBI20110404 Portland Press Limited 2012-05-11 Cancer http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110680 + BMSCs into the tail veins of mice that had received a 65%~70% partial pancreatectomy, while mice that had only received a partial pancreatectomy and mice that had only been injected with BMSCs served as controls. Four weeks later, the injected GFP⁺ BMSCs were diffusely engrafted in the pancreatic parenchyma and mesenchyma of the recipient mice with pancreatic injuries and were differentiated into pancreatic ductal epithelial cells (accounted for 1.7±0.3%), vascular endothelial cells (accounted for 3.2±0.6%) and pancreatic stellate cells (PSCs) (accounted for 5.2±1.6%) but not any pancreatic beta cells or neural cells. Significantly more engrafted and differentiated GFP⁺ BMSCs were observed in the regenerating pancreas than in the normal pancreas. For the mice that received a partial pancreatectomy, the pancreatic weight/body weight of the mice with BMSC treatment ((0.225±0.042)%) was more than that of the mice without BMSC treatment ((0.183±0.021)%) (p<0.05). In addition, real time RT-PCR showed that the expression levels of miR-9 and miR-204 in the engrafted BMSCs (5.2-fold and 2.6-fold, p<0.05, respectively) were increased compared with wild-type BMSCs. We also observed a significant reduction in the expression of miR-375 (0.71-fold, p<0.05) in engrafted GFP⁺ BMSCs compared with wild-type BMSCs. Here, we demonstrate that BMSCs can be a potential cell bank for treating pancreatic injuries by contributing to a variety of cell types; this process might be related to the expression of miR-9, miR-204 and miR-375.]]> F Han, C Wang, L Yang, S Zhan, M Zhang, K Tian 2012-05-11T11:03:26Z doi:10.1042/CBI20110680 Portland Press Limited 2012-05-11 Stem cells http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110146 P Wang, M D. Howard, H Zhang, N Reddy Chintagari, A Bell, N Jin, A Mishra, L Liu 2012-05-10T10:48:26Z doi:10.1042/CBI20110146 Portland Press Limited 2012-05-10 Exo/endocytosis http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110591 F de Assis Nunes Pereira, R L Tavares, A Fernando Camargos, A Lopes da Silva-Filho 2012-05-04T13:13:05Z doi:10.1042/CBI20110591 Portland Press Limited 2012-05-04 Stem cells http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110342 st century, emerging area of systems biology is a whole-istic approach to understand biology by the crosstalk study between genome, Rnome and proteome of a cell. Here we describe a column based rapid method for the simultaneous extraction of nucleic acids, small RNAs and proteins from the same experimental sample (without fractionation) allowing for direct correlations between genomic, epi-genomic, transcriptomic and proteomic data, thus reducing inconsistent results and variability. Our method provides a rapid isolation of crucial biomolecules within one hour with the highest quality of isolated biomolecules. Further isolated DNA, RNA and miRNAs are suitable for all common downstream applications such as PCR, RT-PCR, reverse Northern blotting and Real time PCR. Similarly isolated protein is also suitable for SDS-PAGE and Western blot analysis. The buffers and reagents used in this method are optimized extensively to achieve the cost effective and reliable procedure to separate the functional biomolecules of the cell.]]> S K Rajput, V P Dave, A Rajput, H P Pandey, T K Datta, R K Singh 2012-05-03T13:37:54Z doi:10.1042/CBI20110342 Portland Press Limited 2012-05-03 Trafficking http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110534 X Lou, Y Liu, K Guo, J Lei, H Li 2012-05-03T10:01:10Z doi:10.1042/CBI20110534 Portland Press Limited 2012-05-03 Cancer http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110542 473) of PGCs after stimulation with RA, but this effect was abolished by LY294002 or KP372-1. Meanwhile, treatment with RA increased expression of NF-κB and decreased IκBα expression that were inhibited by SN50. Moreover, blockade of PI3K or Akt activity resulted in inhibiting NF-κB translocation from the cytoplasm to the nucleus. Finally, the up-regulated mRNA expression of cell cycle regulating genes (cyclin D1 and E, cyclin-dependent kinases 6 and 2) was observed in the RA-treated cells. Again, this stimulation was remarkably retarded by combined treatment with LY294002, KP372-1 and SN50, respectively. Therefore, these results suggest that the vitamin A metabolite RA activates the PI3K/Akt and NF-κB signaling cascade to promote proliferation of the cultured chicken PGCs.]]> M Yu, C Ge, W Zeng, Y Mi, C Zhang 2012-05-02T09:57:43Z doi:10.1042/CBI20110542 Portland Press Limited 2012-05-02 Signalling http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20120184 W H Goldmann 2012-04-24T11:10:11Z doi:10.1042/CBI20120184 Portland Press Limited 2012-04-24 Cytoskeleton http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110348 R Biswas Bhattacharjee, T Zannat, J Bag 2012-04-23T10:34:35Z doi:10.1042/CBI20110348 Portland Press Limited 2012-04-23 Cell death http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110368 2+ and Cytochrome C signals in the cytoplasm, as they are important pro-apoptotic signals. The results shows decrease of Ca²⁺ release and up-regulation of Cytochrome C (Cyto C) upon EBV infection. After siRNA transfection, the dysregulatoin of Cyto C was neutralized, which gives the evidence that the level of Cyto C’s release in virus infected NPC cells was as same as that of non-infected NPC cells. This result indicates that EBV infection changes the cytoplasmic level of Cyto C through regulating VDAC1. In summary, this study firstly reports EBV can change the release of Ca²⁺ and Cyto C in the cytoplasm of NPC cells and these changes were mediated by VDAC1 regulation.]]> X Feng, C Ching, W Chen 2012-04-13T11:33:05Z doi:10.1042/CBI20110368 Portland Press Limited 2012-04-13 Cell death http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20100919 +/H⁺ exchanger 1 (NHE1) in this process. The K562 cells were tested for differentiation-related morphological characterization using light microscopy. The fluorescent probe BCECF was used for intracellular pH (pH_i) measurements. Expressions of NHE1 and differentiation-related genes were analyzed by real-time RT-PCR. The cytokine release was determined by protein microarray assay. Signaling pathways were examined by western blotting using phosphospecific antibodies. As a result, hypoxia induced the differentiation of K562 cells as evidenced in the modifications in morphological features, up-regulation of CCAAT/enhancer-binding protein α (C/EBPα), and marked IL-8 release. Inhibition of NHE1 under hypoxia additionally enhanced the levels of C/EBPα and further promoted leukemia cells differentiation. Furthermore, the pharmacological inhibition of p38 mitogen-activated protein kinase (p38 MAPK) significantly suppressed C/EBPα expression under hypoxia conditions after NHE1 inhibition. These results indicate the enhancement of hypoxia-induced K562 differentiation by NHE1 inhibition which may be through the up-regulation of C/EBPα via p38 MAPK signaling pathway, and suggest a possible therapeutic target of NHE1 under hypoxia microenvironment in the treatment of leukemic diseases.]]> W Jin, Q Li, J Wang, G Chang, Y Lin, H Li, L Wang, W Gao, T Pang 2012-04-12T11:01:46Z doi:10.1042/CBI20100919 Portland Press Limited 2012-04-12 Differentiation http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110628 A Mendoza-Naranjo, P Cormie, A E Serrano, C M Wang, C Thrasivoulou, J ES Sutcliffe, D J Gilmartin, J Tsui, T E Serena, A RJ Phillips, D L Becker 2012-03-28T15:32:44Z doi:10.1042/CBI20110628 Portland Press Limited 2012-03-28 Signalling http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110104 Abstract Kupffer cells (KCs), as an important hepatic immunoregulatory cells, play a key role in liver regeneration (LR). Uncovering the transcriptional profiling of KCs after partial hepatectomy (PH) would likely clarify its implication in LR. Here, we isolated KCs by methods of Percoll density gradient centrifugation and immunomagnetic beads. Transcriptional profiles of KCs were monitored up to 168h post-PH using microarray. By comparing the expression profile of KCs at 2-168 h post-PH with that of the control and applying tbe statistical and bioinformatics criteria, we found 1407 known and 927 unknown genes related to LR. K-means clustering analysis grouped these 1407 genes into robust fourteen time-course clusters representing distinct patterns of regulation. Based on gene set enrichment analysis, genes encoding products involved in cytokine signaling, inflammatory response and cell chemotaxis were highly enriched in the cluster characterized by gradual upregulation and then return; genes in defense response and immune response were enriched in clusters “the general down-regulation during LR”; genes in fatty acid synthesis and sterol metabolism were preferentially distributed in the cluster “gradual increase”; while genes in the categories “lipid catabolism” and “glycolysis” were enriched in cluster “decrease at two intervals”. According to above analysis, KCs were seemingly sensitive to operative stimulus; immune defense and detoxification function of KCs obviously dropped postoperatively; fatty acid synthesis were enhanced, while lipid catabolism and glycolysis were reduced after PH. This study provides a detailed in vivo gene expression profile of Kupffer cells, providing a framework to better understand the molecular mechanisms underlying the regeneration process at cellular level.]]> C Xu, X Chen, C Chang, G Wang, W Wang, L Zhang, Q Zhu, L Wang 2012-03-27T14:43:06Z doi:10.1042/CBI20110104 Portland Press Limited 2012-03-27 Division http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110566 60 derivative on the cytotoxicity of a highly reactive free radical nitric oxide (NO) was investigated. Consistent with its cytoprotective abilities, the derivative can scavenge the reactive oxygen species and reactive nitrogen species both in vitro and in cell free condition. Moreover, glutathione C₆₀ derivative protected PC12 cells from the cytotoxic effect of NO-releasing compounds sodium nitroprusside. Experiments also demonstrated that addition of glutathione C₆₀ derivative alone didn’t induce apoptosis and necrosis. The results suggest that glutathione C₆₀ derivative have the potential to prevent NO-mediated cell death without evident toxicity.]]> Z Hu, C Zhang, P Tang, C Li, Y Yao, S Sun, L Zhang, Y Huang 2012-03-22T15:34:02Z doi:10.1042/CBI20110566 Portland Press Limited 2012-03-22 Cell death http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110602 substantia nigra of the midbrain region, but not in the ventral tegmental area and other catecholaminergic cell group areas. The etiology of PD is attributed both to environmental and genetic causes, and certain population of individuals may be classified as at-risk of developing PD later in life. However, there are as yet no therapy regimens that can help to delay or prevent the onset of the disease to realize long-term benefits from this early diagnosis. In PD, a vicious cycle gets initiated in the substantia nigra, due to which susceptible neurons continue to degenerate while damaged neurons do not get enough support for regeneration. This happens primarily due to the local environment of oxidative damage brought about by the dual presence of dopamine and high levels of iron, decline in cellular detoxification systems and low density of glial cells surrounding the dopaminergic neurons in the mesencephalic region. To enhance the defense mechanism of the substantia nigra in this situation, it is necessary to combat the oxidative insult while providing trophic factors for the survival and regeneration of the damaged neurons. In light of in vitro and in vivo studies, mesenchymal stem cells (MSCs) as candidates for cell-based therapies in PD have greater scope than as mere replacement of cell type, since they can be used as a cellular system for the detoxification of ROS as well as a supplier of neurotrophic factors to modulate the local environment. Building on progress in unraveling the multipronged effect of MSCs, we therefore hypothesize that MSCs could be used as a prophylactic strategy to delay or prevent the onset of PD in at-risk individuals, and to slow down the progression of the disease.]]> I Datta, R Bhonde 2012-03-14T16:51:30Z doi:10.1042/CBI20110602 Portland Press Limited 2012-03-14 Stem cells http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110183 M Saba Choudhery, M Khan, R Mahmood, A Mehmood, S N Khan, S Riazuddin 2012-02-22T10:54:14Z doi:10.1042/CBI20110183 Portland Press Limited 2012-02-22 Stem cells http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110595 0/G₁ phase of the cell cycle. Nitric oxide (NO) was not involved in the hUCB-MSC-mediated tumor suppression. The presence of IL-6 and IL-8 were obvious in the hUCB-MSC conditioned media. No significant increase in 29 other cytokines including chemokines, epidermal growth factor, vascular endothelial growth factor (an angiogenic growth factor), TNFR1, TNFRII, adhesion molecules ICAM-1, VCAM-1 and metalloproteinase MMP3 was detected. This is the first report to show that Th1 cytokines, IFN-γ, Th2 cytokine IL-4 and Th17 cytokine, IL-17 were not secreted by hUCB-MSC. hUCB-MSC cocultured with K562 showed an increased number of hUCB-MSC expressing latent membrane-bound form of TGF-β1. The present study indicated that the antiproliferative effect of hUCB-MSC on K562 was due to arrest of the growth of K562 in the G₀/G₁ phase of the cell cycle. The mechanisms underlying the increased IL-6 and IL-8 secretion and LAP(TGF- β1) by hUCB-MSC remains to be investigated.]]> M Fonseka, R Ramasamy, W Kien Yip, B Chong Tan, H Fong Seow 2012-02-16T12:32:12Z doi:10.1042/CBI20110595 Portland Press Limited 2012-02-16 Stem cells http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110111 Z Xiao, M Yang, F Li, Q Lv, Q He, M Deng, X Liu, X Chen, M Chen, X Xie, J Hu 2012-02-02T15:09:56Z doi:10.1042/CBI20110111 Portland Press Limited 2012-02-02 Stem cells http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20100918 50 values were dramatically decreased in cells treated with miR-155 inhibitor combine with taxol, to a greater extent than those treated with taxol alone. Furthermore, the miR-155 inhibitor significantly enhaced apoptosis in U251 cell. Interestingly, the above data suggested that in GBM cells, miR-155 blockage increased the chemosensitivity to taxol. The data strongly suggested that a regulatory loop between miR-155 might provide an insight into the mechanism of modulating EAG1 signaling. Taken together, the miR-155 inhibitor could enhance the chemosensitivity of human glioblastoma cells to taxol. A combination of miR-155 inhibitor and taxol could be an effective therapeutic strategy for controlling the growth of GBM by inhibiting EAG1 expression.]]> w meng, L Jiang, L lu, H Hu, H Yu, D Ding, K Xiao, W Zheng, H Guo, W Ma 2012-01-26T12:01:06Z doi:10.1042/CBI20100918 Portland Press Limited 2012-01-26 Cancer http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20110432 C Rong, F Chen, S Jiang, W Hu, F Wu, T Chen, F Yuan 2011-12-15T11:15:00Z doi:10.1042/CBI20110432 Portland Press Limited 2011-12-15 Cell death http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20100649 K Sankaranarayanan, C T., G Ponrose G., M V., P U., C Maria Renny, U Raghavan, S R., S Guhathakurta, C K. M. 2011-04-15T09:27:47Z doi:10.1042/CBI20100649 Portland Press Limited 2011-04-15 Stem cells http://www.cellbiolint.org/cbi/imps/refer.htm?MSID=CBI20090021 D Ou, R Chen, X Liu, J Guo, H Wang, Q Zheng 2009-09-15T15:09:57Z doi:10.1042/CBI20090021 Portland Press Limited 2009-09-15 Stem cells