It will be interesting to further explore specific phospho sites

Posted on May 14, 2015 by admin

It will be interesting to further explore specific phospho sites involved in imparting stability to DNMT1 and DNMT3B and the kinases responsible CC5013 for this phosphorylation. Conclusions In summary, the data presented in this report indicates that mahanine selectively degrades DNMT1 and DNM T3B via the ubiquitin proteasomal pathway in a manner dependent on the inactivation of Akt signaling. The degradation Inhibitors,Modulators,Libraries of DNMT1 and DNMT3B prompts the demethylation of the promoter of the silenced tumour suppressor gene RASSF1A, leading to the restoration of its expression in prostate cancer cells. There fore, mahanine could potentially be used in the therapy of advanced prostate cancer in men when RASSF1A ex pression is silenced.

Methods Mahanine purification, cell culture, and cell transfection Mahanine was purified from the leaves of Murraya koenigii as described in our previous published report. Human prostate cancer cell lines, PC3 and LNCaP were obtained from American Type Culture Collection. Cells Inhibitors,Modulators,Libraries were grown in IMEM containing 10% fetal bovine serum, 2 mM Inhibitors,Modulators,Libraries glutamine, 100 uml penicil lin G sodium, and 100 mgml streptomycin sulfate at 37 C and 5% CO2. BPH1 cells were obtained from Dr. Simon W. Hayward of Vanderbilt University and cul tured in the same medium as mentioned above. PC3 cells were transfected with DNMT shRNAs and RASS F1A expression vector. BPH1 cells were transfected with 1ugml of DNMT expression vectors or constitutively active Akt 17 254 plasmids using Genjet vII reagent. Forty eight hours after transfection, cells were harvested for RT PCR analyses.

Live and dead cells were determined according to the manufacturers instructions Western blot analysis Western blot analysis was performed according to our earlier published report. In brief, After 24 hours of mahanine, wortmannin, and MG132 treatment, cellular protein extracts were prepared from PC3 and Inhibitors,Modulators,Libraries LNCaP cells after various treatments of mahanine, wortmannin, and MG132. Fifty micrograms of proteins were resolved on 8% SDS PAGE and transferred onto nitrocellulose membranes, and immunoblot ted with primary antibodies overnight at 4 C. Immunoreactive protein bands were detected with horseradish peroxidise conjugated secondary antibodies and with enhanced chemiluminescence system accord ing to the manufacturers instructions. Band intensities were quantified by ImageJ software.

The pre paration of nuclear extracts and immunoprecipitations were performed Inhibitors,Modulators,Libraries according to our previously published methods. Immunofluorescence selleck chemical Rapamycin staining Immunofluorescence staining was performed according to our previously published report. PC3 cells were plated onto ECL coated chamber slides and were treated with mahanine, wortmannin, or DMSO as controls. The cells were fixed in ?20 C methanol, air dried, and re hydrated in PBS.

The identified biclusters are biologically relevant to the develo

Posted on May 13, 2015 by admin

The identified biclusters are biologically relevant to the development stages in vivo. Group VE-822? 1 contains endoderm Inhibitors,Modulators,Libraries markers CER and HNF6 under FGF2WNT3A and BMP4WNT3API3KI. CER is an important early mar ker for the DE stage rising after the formation of the primitive streak during development while HNF6 is a marker for a more primitive foregut stage in pancreas development. Thus, Group 1 is similar to the foregut development stage in vivo. In addition, the condi tions in Group 1 contain FGF2 and WNT3A but not BMP4 and as seen from Figure 5, CER and HNF6 decrease under BMP4 dominance. Thus, the biclustering analysis shows that the early marker CER and a late endoderm marker HNF6 are controlled by the FGF2, WNT3A pathway and are relatively down regulated under BMP4 and PI3KI.

Group 2 contains another primitive foregut stage Inhibitors,Modulators,Libraries marker HNF4 along with HNF6. Interestingly here, the biclustering results show that pancreatic endodermal transcriptional machinery may not be favored at the DE stage by the FGF2 BMP4 combination although in our hierarchical clustering results FGF2 BMP4 combination clustered with the other conditions that gave a better DE signature. We also note that WNT3A and PI3KI combination with high activin increased the expression of HNF4 and HNF6 and these conditions also gave a successful DE signature as seen from the hierarchical clustering. Thus our results indicate that WNT3A pathway can favor both early and late markers like CER, HNF4 and HNF6. Also, WNT3A PI3KI induced DE cells may be more capable of developing into later pancreatic lineages.

While WNT3A and PI3KI have been used for DE induc tion towards pancreatic maturation, the effect of co induction has not been explored yet. Discussion The differentiation of hESCs into Inhibitors,Modulators,Libraries the endoderm lineages is carried out by the activation of different signaling pathways mimicking in vivo development. However, there is no consensus on which induction method is the most desirable and whether combination of these could result in an endoderm with the best signature. Here, we have used a combination Inhibitors,Modulators,Libraries of experimental and mathemat ical techniques to shed light on these concerns. The DE signature differs under exogenous activation of different signaling pathways participating in endoderm commitment Our experiments with different DE inducing conditions show that the DE potential of the differentiating hESCs is highly dependent on the method of DE induction.

The major DE markers showed considerable variation when some of the path ways were activated above their basal levels. All the pathways studied here have been Inhibitors,Modulators,Libraries known to be important at the earlier stages of especially in vivo endoderm dif ferentiation and has also been documented as necessary for in vitro differentiation. The common de nominator in our studies is activin A which is an essen tial inducer of DE.

Conclusions In summary, activated T cells express CYP27B1 and can

Posted on May 12, 2015 by admin

Conclusions In summary, activated T cells express CYP27B1 and can convert 25 D3 to 1,25 2D3 in sufficiently high concentrations to affect vitamin D responsive genes when cultured in serum free medium. However, DBP sequesters 25 D3 and inhibits the production of 1,25 2D3 in T cells. To fully exploit the immune regulatory potential of vitamin D, further studies of most the mechanisms that en able the immune system to Inhibitors,Modulators,Libraries exploit 25 D3 and convert it to 1,25 2D3 are required. Methods Chemicals were prepared in anhydrous ethanol and stored at ?80 C. To determine 1,25 2D3 in the medium we used the 1,25 Dihydroxy Vita min D EIA kit from IDS, Tyne and Wear, UK according to the manufacturers instructions. DBP and albumin purified from human serum were from Meridian Life Sciences and Sigma Aldrich, respectively.

Actin, arachidonic acid and ketoconazole were from Sigma Aldrich. Serum and central lymph from mini pigs were provided by the Department for Experimental Medicine, University of Copenhagen, Denmark. Cell culture Mononuclear cells from blood were isolated by Lympho prep Inhibitors,Modulators,Libraries density gradient centri fugation from healthy donors after obtaining informed, written consent in accordance with the Declarations of Helsinki principles for research involving human objects. The study was approved by the local Ethics Committee. Na ve CD4 T cells were isolated, cultured and activated as previously described. The cells were activated for 3 days in serum free X VIVO 15 medium if not otherwise stated. Flow cytometry For flow cytometry analyses of CD38 and TCR expres sion the cells were stained with anti CD38 APC both Inhibitors,Modulators,Libraries from BD Biosciences and analyzed on a FACS Calibur.

Fold change in CD38 surface expression was calculated as mean CD38 fluores cence intensity of cells stimulated in the presence of divided with mean CD38 fluores cence intensity Inhibitors,Modulators,Libraries of cells stimulated in the absence Percent TCR surface expression was calculated as Western blot and Inhibitors,Modulators,Libraries ELISA Western blot analyses were performed as previously described. Following incubation with primary antibody, the membranes were washed, and the pro teins visualized following 60 min incubation at room temperature with HRP conjugated sellckchem rabbit anti mouse Ig, swine anti rabbit Ig or rabbit anti goat Ig using ECL technology. The primary antibodies used were anti ezrin and anti DBP. For band density quantification ECL exposed sheets were analysed in a ChemiDoc MP Imaging System from Bio Rad. Meas urement of the cytokines IL 13 and IFN were deter mined by ELISA according to the manufacturers protocol.

Although to date, few randomized phase III melanoma trials have s

Posted on May 11, 2015 by admin

Although to date, few randomized phase III melanoma trials have shown clinical benefit, post hoc analysis of some trials, which buy inhibitor overall were negative, did reveal statistically significant benefits in favor of the inves tigational arm for melanoma patients with normal versus high serum LDH. The SYMMETRY study, a randomized phase III trial that determined efficacy of the small molecule inhibitor Elesclomol, administered alone or in combination with paclitaxel, provided evidence that while the combination of Elesclomol with paclitaxel led to significant progression free survival in patients with normal serum LDH, there was a trend towards worse overall survival in patients with high serum LDH. We and others have shown that Elesclomol suppresses OXPHOS in melanoma cells in vitro, and that melanoma cells without mitochondrial DNA are more resistant to low to moderate doses of Elesclomol.

These findings, in addition to the critical role of LDH in the interconversion of lactate and pyruvate in the production of ATP through glycolysis or OXPHOS, prompted us to hypothesize that Inhibitors,Modulators,Libraries differences in serum LDH among patients with metastatic melanoma reflect differential dependence Inhibitors,Modulators,Libraries upon these bioenergetic pathways. In view of these observations we sought to determine whether 1) the LDH isoform expression profile and levels of lactate in serum obtained from up to 49 patients with metastatic melanoma would correlate with disease progression and OS. and 2) whether melanoma development and progression might be linked with key enzymes in glycolysis, OXPHOS, and lactate transport.

Our data presented herein demonstrate that patients with advanced metastatic melanoma and high serum LDH have low levels of LDH1 and LDH2, but elevated levels of LDH3 and 4, suggesting that glycolysis is the primary metabolic pathway utilized by the tumor cells in Inhibitors,Modulators,Libraries these patients. In contrast, in patients with advanced melanoma and normal serum LDH, OXPHOS has an important role in addition to glycolysis for energy production. Furthermore, our data demonstrate that several key enzymes associated with high OXPHOS are substantially elevated in primary and metastatic melanomas compared with nevic melanocytes. Together these findings support a model that both glycolysis and OXPHOS play a significant role in developing metabolic symbiosis in metastatic melanoma progression.

Materials and methods Inhibitors,Modulators,Libraries Patient sera, melanoma cell lines, and tumor cell suspensions Sera from patients with stage IV metastatic melanoma were obtained in compliance with University of Pittsburgh Cancer Institute protocols 96 099 and 11 108. Overall Inhibitors,Modulators,Libraries survival was defined as the interval from collection of serum LDH, LDH isoenzyme, and serum thereby lactate to death from any cause. Human epidermal melanocytes were propagated in melanocyte growth medium.

The amplified TRAIL induced caspase activation by overexpressed c

Posted on May 8, 2015 by admin

The amplified TRAIL induced caspase activation by overexpressed c Myc counteract the anti apoptotic activity of DNA PKcs by increasing proteolytic cleavage in the metastatic cancer cells It has been known that a constitutively active Akt is an important Tofacitinib baldness regulator of TRAIL sensitivity, and inhibition of Akt activation by its pharmacological inhi bitor or knockdown Inhibitors,Modulators,Libraries of its expression by siRNA sensi tizes TRAIL resistant cells to TRAIL. The activation of Akt Inhibitors,Modulators,Libraries by phosphorylation of Ser 473 is mediated by DNA PKcs. However, the metastatic cancer cells were sensitive to TRAIL, despite that the metastatic cells have higher level of DNA PKcs com pared with their primary cells, as shown above. There fore, we determined the levels of DNA PKcs and pAkt in the metastatic cells after treatment with TRAIL.

In metastatic PC3 MM2 and KM12L4A cells, DNA PKcs was cleaved and consequently the level of DNA PKcs was decreased after exposure to TRAIL and this result was accompanied with decrease of pAkt level, whereas the levels of DNA PKcs and pAkt were maintained in the primary PC3 and KM12 cells after Inhibitors,Modulators,Libraries exposure to TRAIL. Since c Myc could control the TRAIL sensitivity, and DNA PKcs is a substrate of caspase 3, we deter mined whether depletion of c Myc could block degrada tion of DNA PKcs. When PC3 MM2 cells were transfected with c Myc siRNA, TRAIL induced cleavage of DNA PKcs was reduced compared with transfection with scrambled siRNA. These results were followed by prevention of cleavage of DNA PKcs as well as PARP in the TRAIL treated cells by pretreatment with Z DEVD FMK, a caspase 3 specific inhibitor.

Inhibitors,Modulators,Libraries These Inhibitors,Modulators,Libraries results suggest that the amplified TRAIL induced cas pase activation by over expressed c Myc may curtail the anti apoptotic activity of DNA PKcs by increasing its proteolytic cleavage in the metastatic cancer cells. Suppression of DNA PKcs is associated with hypersensitivity to TRAIL induced cytotoxicity To investigate the direct role of DNA PKcs in the sus ceptibility of the metastatic cells to TRAIL, we used siRNA to knockdown DNA PKcs expression and deter mined its effect on TRAIL sensitivity. After transfection of PC3 or KM12 cells with siRNA against DNA PKcs or scrambled siRNA, the expression of DNA PKcs was effi ciently suppressed by DNA PKcs siRNA as compared to the control cells and its expression was further decreased by TRAIL treatment.

This result was followed by the hypersensitivity to TRAIL induced reduction of DNA PKcs/pAkt levels, activation of cas pases, PARP cleavage, and up regulation of Bax in PC3 and KM12 cells after transfection those with DNA PKcs siRNA as compared to the cells transfected with scrambled siRNA. Furthermore, the knockdown of DNA PKcs with specific siRNA significantly increased TRAIL induced apoptosis in PC3 and KM12 cells.

Posted on May 7, 2015 by admin

ABT888 As shown in Fig. 5C, Inhibitors,Modulators,Libraries MET silencing strongly delayed tumor onset in mice injected with control cells. In fact, after 40 days of MET silencing, the incidence of visible tumors was only 20%. However, Inhibitors,Modulators,Libraries tumors expressing EGFR Inhibitors,Modulators,Libraries L858R or having the TGF autocrine production were considerably resistant to MET silencing, as demon strated by a complete rescue in tumor incidence. The expression of EGFR L858R or TGF does not signif icantly promote tumor growth in untreated cells. These data demonstrate that activat ing mutations of EGFR and TGF autocrine loop can impair the effect of MET silencing in vivo. HER family members contribute to the onset of secondary resistance to MET inhibition To verify if HER members are involved in secondary resistance to MET inhibition, we continuously treated GTL16 cells with a dose of 500 nM PHA, mimicking a hypothetical clinical treatment regimen.

After few months of PHA administration, cells developed resis tance to the Inhibitors,Modulators,Libraries drug. In fact, while GTL16 parental cells treated with 500 nM PHA displayed an almost complete abrogation of growth, the resistant cells were only slightly affected by PHA. The anal ysis of Inhibitors,Modulators,Libraries these cells revealed that the MET gene was neither mutated nor amplified, and that other master regulators of cell proliferation, such as H RAS and K RAS, B Raf and PI3KCA had none of the known mutations. We then analyzed the HER family status, finding that the resistant cells showed a significant increase in the expression level of these receptors, compared to parental cells. No muta tions neither gene amplification were present in EGFR.

In order to verify if the overexpression of HER2 and HER3 could be responsible, therefore at least partially, for the development of resistance, we silenced both receptors in parental and in resistant cells and tested the viability of these cells in the absence or presence of PHA. Interestingly, we observed that HER2/HER3 silencing significantly reduced the ability of resistant cells to grow in the pres ence of PHA, with no significant effect on the parental counterpart. Collectively, these findings demonstrate that alterations in HER family members can actually contribute to the onset of secondary resistance to PHA in initially respon sive tumor cells. Discussion The clinical experience derived from use of drugs target ing molecules that play critical roles in human tumors has shown that their efficacy critically depends on the pres ence of the altered target in the neoplasm.

However, even in these conditions, a response to the inhibitor is seen only in a fraction of patients. Moreover, even in responding patients in which the drugs are initially successful in impairing tumor growth, their efficacy decreases or is abrogated in a short time period, due to appearance of secondary resistance.

5 irradiated mouse embryonic fibroblasts All animal research was

Posted on May 6, 2015 by admin

5 irradiated mouse embryonic fibroblasts. All animal research was performed at the Animal Care Facility of the Research Institute of Childrens Hospital Los Angeles in accordance selleckbio with institutional guidelines. Ani mals were maintained in accordance with the NIH Guide for the care and use of Laboratory Inhibitors,Modulators,Libraries Animals. Treatment of lymphoblastic leukemia cells with Nilotinib,imatinib neither or AG490 Nilotinib was obtained from Novartis Pharmaceuticals. AG490 was purchased from Calbio chem. The parental lymphoblastic leukemia cell line 8093 and the A 5 and A 21 cell lines were seeded in wells of a 6 well plate either in the presence or absence of E14. 5 irradiated MEFs as described. Samples in triplicate wells were treated either with 20,50,100,or 200 nM nilotinib or 5M imat inib or DMSO as control.

In additional pilot experiments,8093 cells were treated with 100,75,50 Inhibitors,Modulators,Libraries and 5M AG490 while cultured on MEFs. The cell viability in control exper iments Inhibitors,Modulators,Libraries Inhibitors,Modulators,Libraries Inhibitors,Modulators,Libraries was consistently above 80%. Drug in the experi mental wells was added every second or third day along with the fresh Inhibitors,Modulators,Libraries change of medium dependent on prolifera tion of the treated cells. Aliquots were removed from each individual well and cell viability was determined using the Trypan Blue exclusion method. Viability is expressed as percentage of the number of Trypan Inhibitors,Modulators,Libraries Blue excluding cells divided by the number of total cells. In the case of AG490 treatment,viability was measured Inhibitors,Modulators,Libraries by propidium iodide uptake using a FACScan.

Each data point is represented as mean SEM of triplicate samples.

Treatment with nilotinib in a transplant model Fifteen C57Bl 6J mice were transplanted with 1 �� 104 8093 Inhibitors,Modulators,Libraries cells via a tail vein injection. Five days later,mice were Inhibitors,Modulators,Libraries ran domly selected for vehicle or nilotinib treatment. Eight mice were fed a mixture of 8 parts peanut butter and two parts vegetable www.selleckchem.com/products/Calcitriol-(Rocaltrol).html oil and the remaining seven mice were treated with 75 mg of nilotinib kg body weight added to the same peanut oil mixture daily. Treatment was stopped 50 days after day 1 of transplantation. Analysis of leukemia regression in transgenic mice treated with nilotinib Peripheral blood of preleukemic and overtly leukemic P190 transgenic mice as well as wild type littermates was examined by flow cytometry using a FACScan to identify markers suitable to detect the leukemic cells. Peripheral blood of three additional P190 transgenic animals that had developed overt leukemia lymphoma was analyzed before and after seven days of treatment with nilotinib as described above. After erythrocyte lysis,cells were stained with antibodies Crizotinib NSCLC against mouse CD19 and AA4. 1.

AP2 and Sp1

Posted on May 5, 2015 by admin

AP2 and Sp1 Ganetespib clinical trial are two transcription factors www.selleckchem.com/products/baricitinib-ly3009104.html mainly con trolled by Ras Raf ERKs pathway activation. In order to measure the pathway activity, we first measured Ras protein activity levels able to stimulate the ERK cas MG132 proteasome cade. ASP13 clone showed an increased capacity to acti vate Raf that was associated with increased pERK levels, while no differences were ob served on PI3K cascade measured Inhibitors,Modulators,Libraries by pAKT levels. Accordingly, when ERKs activity was inhibited with U0126 for 15 minutes, Inhibitors,Modulators,Libraries a decay in mRNA VEGF A levels was observed in ASP13 clone that was not evident in CYS12. No differences in total Sp1 protein levels were observed in mutants clones ASP13 or CYS12.

In all, these results indicate that Ras Raf ERK AP2/Sp1 Inhibitors,Modulators,Libraries signalling cascade is responsible for VEGF A overexpression in ASP13 cells.

To study if these differences detected in vitro could cause a difference in the angiogenic Inhibitors,Modulators,Libraries patterns and tu Inhibitors,Modulators,Libraries moral capacity we subcutaneously injected NIH3T3 con trol cells and transfected clones in nude mice. In agreement with our previous Inhibitors,Modulators,Libraries Inhibitors,Modulators,Libraries observations latency period of tumors arising from Inhibitors,Modulators,Libraries distinct ASP13 transfectants was longer than Inhibitors,Modulators,Libraries Inhibitors,Modulators,Libraries for CYS12 tumors HIF 1 activity and hypoxia was assessed though immu nostaining of GLUT 1 and Carbonic Anhydrase IX. In concordance with in vitro observations, GLUT 1 immu nostaining was more intense in CYS12 tumors Inhibitors,Modulators,Libraries albeit the percentage of positive cells did not among the two transfectants.

Differences in the expression of Carbonic Anhydrase Inhibitors,Modulators,Libraries IX were more Inhibitors,Modulators,Libraries intense, being the percentage of positive cells 4 times higher in CYS12 tumors.

We confirmed that mRNA VEGF A levels were also higher in ASP13 tumours compared Inhibitors,Modulators,Libraries with CYS12. The same trend was observed at the protein VEGF A level, as assessed by ELISA and immunostaining. In contrast, angiogenic Cisplatin side effects factor Angiopoietin 2 levels did not show differences between tumours. Tumor growth vascular patterns The distinct VEGF A production observed was associ ated with a specific vascular pattern. On the one hand, vascular hotspots zones with distended vessels were apparent in ASP13 tumours, with generation of haemorragic and necrosis zones.

On the other Inhibitors,Modulators,Libraries hand, microvessel density was higher in CYS12, being the diameter of vessels higher in ASP13 tumours.

Finally, vessels from ASP13 tumours were surrounded by Y-27632 msds mural cells that stained positive for Smooth Muscle Actin and Desmin proteins, while mural cells were scarce around CYS12 tortuous vessels. These different vascular patterns do not associate with significant differences in the degree of necrosis among the two transfectants. Discussion In the context of KRAS driven tumourigenesis, mutations located at codon 12 and 13 display distinct malignant potential and differentially regulate apoptosis, cell cycle, or metabolic small molecule profiles.

Conclusion In this work,

Posted on May 4, 2015 by admin

Conclusion In this work, kinase inhibitor Ivacaftor Inhibitors,Modulators,Libraries regression analysis was used to determine how cell signaling correlates with castration resistant growth across three cell lines. Based on the data presented, in vitro prostate cancer cell androgen independent growth could be largely described via MAPK and PI3K signaling. Androgen mediated signaling also largely acted through PI3K signaling. p JNK appeared to potentially play a role in the fundamental cas tration resistance of a cell line, and MDA PCa 2b cells did not utilize p Erk to enable androgen independent growth. Given the myriad of targeted inhibitors currently in devel opment, approaches similar to this work which determine drivers of disease progression may enable optimizing treatment given the unique signaling of each patient.

Background Inhibitors,Modulators,Libraries Aside from non melanoma skin cancers, breast cancer is the most common cancer among women worldwide, with nearly 1. 4 million new cases diagnosed in 2008. Often, breast cancers are characterized by their expression of hormone receptors. Cancers expressing one or more of these recep tors have the potential to be treated with targeted therap ies, including tamoxifen and trastuzumab. On the other hand, there is no specific treatment regimen for patients whose cancers lack these three receptors, so called triple negative breast cancers, which tend to be clinic ally aggressive with a trend of poorer outcomes. Thus, it is critical to develop and explore therapeutic options that may be of use to these patients. Aminoflavone 6,8 difluoro 7 methyl, Inhibitors,Modulators,Libraries NSC 686288 is a synthetic flavonoid compound.

Similar compounds are frequently found in fruits and vegetables, and Inhibitors,Modulators,Libraries have a variety of effects within the body, including reported cytostatic, apoptotic, anti inflammatory, anti angiogenic, and estrogenic activities. The National Cancer Institutes 60 human tumor cell line anticancer drug screen revealed that AF mediated growth inhibition in numerous renal, breast and ovarian tumor cell lines, and produced a unique fingerprint of activity in the COMPARE algorithm, unlike any other group of anti tumor compounds. A pattern uncovered in AFs differential activity in human breast cancer cell lines was the exquisite sensitivity of cells expressing estrogen Inhibitors,Modulators,Libraries re ceptor alpha, such as MCF7 and T47D, and resist ance exhibited by cells lacking ER expression, including MDA MB 231, Hs578T, and BT 549.

When mice bear ing ER positive MCF7 xenografts were treated with AF, tumor growth was inhibited. Further, it has been shown that AF resistant and ER negative cell lines MDA MB 231 and Hs578T may be re sensitized to AF through co treatment with vorinostat, Tofacitinib Citrate which reactivates ER expression and AhR mediated CYP1A1 activity. These data imply that ER positive cancers might ex hibit enhanced sensitivity to AF as compared with ER negative cancers.

MiRna Assay

MiRNA or precursor miRNA assays for microRNA research

Monthly Archives: May 2015