Specialized antibody services, Conjugation.

An article published this year in “THE JOURNAL OF IMMUNOLOGY” using our Specialized Antibody Services for Anti– TNF-a directly labeling with CF-Blue, by our customers from University Pompeu Fabra,, Hospital del Mar Medical Research Institute and Department of Immunology, Hospital del Mar, Barcelona, Spain, in the analysis of how Antibody-Dependent NK Cell Activation Differentially Targets EBV-Infected Cells in Lytic Cycle and Bystander B Lymphocytes Bound to Viral Antigen–Containing Particles. Congrats and Thanks.

Summary:

NK cells have been reported to respond against EBV-infected B cells in the lytic cycle and to control the viral infection involving IFN-γ secretion. Early reports proposed a role for NK cell Ab-dependent cellular cytotoxicity (ADCC) triggered via FcγR-IIIA (CD16) in the response to EBV. In the current study, we revisited this issue, showing that serum from EBV+ individuals triggered vigorous NK cell degranulation and cytokine production (i.e., TNF-α and IFN-γ) against EBV-infected cells, enhancing NK cell activation. The effect was preferentially directed against cells in the lytic phase and was associated with surface expression of the gp350/220 envelope Ag. In contrast, binding of gp350+ particles, released by EBV-infected cells, to B cell lines or autologous primary B lymphocytes also promoted specific Ab-dependent NK cell degranulation and TNF-α production but induced minimal IFN-γ secretion. In that case, target cell damage appeared marginal compared with the effect of a control anti-CD20 Ab (rituximab) at concentrations that triggered similar NK cell activation, indicating that cell-associated gp350+ particles may divert the cytolytic machinery, impairing its direct action on the plasma membrane. These observations support that Ab-dependent NK cell activation plays an important role in the control of EBV, enhancing NK cell effector functions against infected B cells in the lytic cycle. In contrast, the data reveal that gp350+ particles bound to bystander B cells trigger Ab-dependent NK cell degranulation and TNF-α but not cytotoxicity or IFN-γ production, potentially favoring the progression of viral infection.

Reference:

http://www.jimmunol.org/content/early/2017/06/17/jimmunol.1601574

Product link:

Specialized antibody services, Conjugation: http://www.immunostep.com/content/30-specialized-antibody-services

RNase solution and annexin V-fluorescein isothiocyanate (FITC)/PI double staining kit.

An article published this year in “INVESTIGATIONAL NEW DRUGS” using our RNase solution and annexin V-fluorescein isothiocyanate (FITC)/PI double staining kit, by our customers from CNC.IBILI University of Coimbra, Portugal, in the analysis of how Urolithins impair cell proliferation, arrest the cell cycle and induce apoptosis in UMUC3 bladder cancer cells. Congrats and Thanks.

Summary:

Ellagitannins have been gaining attention as potential anticancer molecules. However, the low bioavailability of ellagitannins and their extensive metabolization in the gastrointestinal tract into ellagic acid and urolithins suggest that the health benefits of consuming ellagitannins rely on the direct effects of their metabolites. Recently, chemopreventive and chemotherapeutic activities were ascribed to urolithins. Nonetheless, there is still a need to screen and evaluate the selectivity of these molecules and to elucidate their cellular mechanisms of action. Therefore, this work focused on the antiproliferative effects of urolithins A, B and C and ellagic acid on different human tumor cell lines. The evaluation of cell viability and the determination of the half-maximal inhibitory concentrations indicated that the sensitivity to the studied urolithins varied markedly between the different cell lines, with the bladder cancer cells (UMUC3) being the most susceptible. In UMUC3 cells, urolithin A was the most active molecule, promoting cell cycle arrest at the G2/M checkpoint, increasing apoptotic cell death and inhibiting PI3K/Akt and MAPK signaling. Overall, the present study emphasizes the chemopreventive/chemotherapeutic potential of urolithins, highlighting the stronger effects of urolithin A and its potential to target transitional bladder cancer cells.

Reference:

https://link.springer.com/article/10.1007/s10637-017-0483-7

Product link:

CELL CYCLE ANALYSIS (PI / RNASE): http://www.immunostep.com/solutions-buffers-chemicals/3870-pi-rnase-solution.html

FITC Annexin V Apoptosis Detection Kit with PI: http://www.immunostep.com/apoptosis-tools/3727-anxvkf-100t.html

Cell Cycle Analysis (PI / RNASE) and FITC-conjugated Annexin-V.

An article published this year in “JOURNAL OF HEMATOLOGY & ONCOLOGY” using our Cell Cycle Analysis (PI / RNASE) and our FITC-conjugated Annexin-V, by our customers from University Hospital of Salamanca (IBSAL) & Cancer Research Center (IBMCC-CSIC-USAL), Salamanca, Spain, in the analysis of Preclinical anti-myeloma activity of EDO-S101, a new bendamustine-derived molecule with added HDACi activity, through potent DNA damage induction and impairment of DNA repair. Congrats and Thanks.

Summary:

Background: Despite recent advances in the treatment of multiple myeloma (MM), the prognosis of most patients remains poor, and resistance to traditional and new drugs frequently occurs. EDO-S101 is a novel therapeutic agent conceived as the fusion of a histone deacetylase inhibitor radical to bendamustine, with the aim of potentiating its alkylating activity.

Methods: The efficacy of EDO-S101 was evaluated in vitro, ex vivo and in vivo, alone, and in combination with standard anti-myeloma agents. The underlying mechanisms of action were also evaluated on MM cell lines, patient samples, and different murine models.

Results: EDO-S101 displayed potent activity in vitro in MM cell lines (IC50 1.6–4.8 μM) and ex vivo in cells isolated from MM patients, which was higher than that of bendamustine and independent of the p53 status and previous melphalan resistance. This activity was confirmed in vivo, in a CB17-SCID murine plasmacytoma model and in de novo Vk*MYC mice, leading to a significant survival improvement in both models. In addition, EDO-S101 was the only drug with single-agent activity in the multidrug resistant Vk12653 murine model. Attending to its mechanism of action, the molecule showed both, a HDACi effect (demonstrated by α-tubulin and histone hyperacetylation) and a DNA-damaging effect (shown by an increase in γH2AX); the latter being again clearly more potent than that of bendamustine. Using a reporter plasmid integrated into the genome of some MM cell lines, we demonstrate that, apart from inducing a potent DNA damage, EDO-S101 specifically inhibited the double strand break repair by the homologous recombination pathway. Moreover, EDO-S101 treatment reduced the recruitment of repair proteins such as RAD51 to DNA-damage sites identified as γH2AX foci. Finally, EDO-S101 preclinically synergized with bortezomib, both in vitro and in vivo.

Conclusion: These findings provide rationale for the clinical investigation of EDO-S101 in MM, either as a single agent or in combination with other anti-MM drugs, particularly proteasome inhibitors.

Reference:

https://jhoonline.biomedcentral.com/articles/10.1186/s13045-017-0495-y

Product link:

CELL CYCLE ANALYSIS (PI / RNASE): http://www.immunostep.com/solutions-buffers-chemicals/3870-pi-rnase-solution.html

FITC Annexin V Apoptosis Detection Kit with PI: http://www.immunostep.com/apoptosis-tools/3727-anxvkf-100t.html

FITC Annexin V Apoptosis Detection Kit with 7-AAD.

An article published this year in “ODONTOLOGY” using our FITC-conjugated Annexin-V and 7-AAD, by our customers from Cellular Therapy and Hematopoietic Transplant Unit, Haematology Department, Virgen de la Arrixaca Clinical University Hospital, IMIB, University of Murcia, Spain, in the analysis of Biological effects of silk fibroin 3D scaffolds on stem cells from human exfoliated deciduous teeth (SHEDs). Congrats and Thanks.

Summary:

The aim is to investigate in vitro biological effects of silk fibroin 3D scaffolds on stem cells from human exfoliated deciduous teeth (SHEDs) in terms of proliferation, morphological appearance, cell viability, and expression of mesenchymal stem cell markers. Silk fibroin 3D scaffolding materials may represent promising suitable scaffolds for their application in regenerative endodontic therapy approaches. SHEDs were cultured in silk fibroin 3D scaffolds. Then, cell numbers were counted and the Alamar blue colorimetric assay was used to analyse cell proliferation after 24, 48, 72, and 168 h of culture. The morphological features of SHEDs cultured on silk fibroin scaffolds were evaluated by scanning electron microscopy (SEM). Finally, cell viability and the expression of mesenchymal stem cell markers were analysed by flow cytometry. One-way analysis of variance (ANOVA) followed by a Bonferroni post-test was performed (P < 0.05). At 24 and 48 h of culture, SHED proliferation on scaffolds was modest compared to the control although still significant (p < 0.05). However, cell proliferation progressively increased from 72 to 168 h compared with the control (p < 0.001; p < 0.01). In addition, flow cytometry analysis showed that the culture of SHEDs on silk fibroin scaffolds did not significantly alter the level of expression of the mesenchymal markers CD73, CD90, or CD105 up to 168 h; in addition, cell viability in silk fibroin was similar to than obtained in plastic. Moreover, SEM studies revealed a suitable degree of proliferation, cell spreading, and attachment, especially after 168 h of culture. The findings from the current study suggest that silk fibroin 3D scaffolds had a favourable effect on the biological responses of SHEDs. Further in vivo investigations are required to confirm these results.

Reference:

https://link.springer.com/article/10.1007/s10266-017-0310-9

Product link:

FITC Annexin V Apoptosis Detection Kit with 7-AAD: http://www.immunostep.com/apoptosis-tools/3741-anxvkf-100t.html

PI/RNASE Kit Solution and Annexin V-FITC Apoptosis Detection kit.

An article published this year in “BIOCHIMIE” using our PI/RNASE Kit Solution and Annexin V-FITC Apoptosis Detection kit, by our customers from Laboratório de Oncologia Experimental e Hemopatias, Departamento de Análises Clínicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil, in the analysis of Cytotoxic effect of a novel naphthylchalcone against multiple cancer cells focusing on hematologic malignancies. Congrats and Thanks.

Summary:

Chalcones are natural compounds described in the literature by its several properties including cytotoxic activity against several tumor types. Considering that the search for new chemotherapeutic agents is still necessary, the aim of this study was to investigate the cytotoxic mechanisms involved in cell death induced by a synthetic chalcone (A23) on different tumor cells. Chalcone A23 reduced the cell viability of twelve tumor cell lines in a concentration and time dependent manner and it was more cytotoxic against acute leukemia cells. Interestingly, the compound was non cytotoxic to normal cells and non-hemolytic to normal red blood cells. Chalcone A23 decreased the expression of cell proliferation marker KI-67 and blocked the G2/M phase in both K562 and Jurkat cell lines. Cells treated with A23 showed morphological features suggestive of apoptosis, the “latter pattern” in agarose gel, the externalization of phosphatidylserine and caspase-3 and PARP cleavage. Chalcone A23 significantly reduced the mitochondrial membrane potential, decreased the expression of anti-apoptotic proteins Bcl-2 and survivin and increased the expression of pro-apoptotic protein Bax, confirming the involvement of the intrinsic pathway. The increased mitochondrial permeability resulted in the release of AIF, cytochrome c and endonuclease G from the mitochondria to the cytosol. In addition, chalcone A23 increased the expression of FasR and induced Bid cleavage, showing the involvement of the extrinsic pathway. Finally, chalcone A23 seems to have a synergic effect with the chemotherapy drugs cytarabine and vincristine. These results suggest that A23 is an interesting compound with strong and selective anti-tumor activity.

Reference:

http://www.sciencedirect.com/science/article/pii/S0300908417301487

Product link:

PI/RNASE Kit Solution: http://www.immunostep.com/solutions-buffers-chemicals/3870-pi-rnase-solution.html

Annexin V-FITC Apoptosis Detection kit: http://www.immunostep.com/apoptosis-tools/3727-anxvkf-100t.html

Peptide Production Service.

An article published this year in “NANOMEDICINE” using our Peptide Production Service, by our customers from Immunology Division, Germans Trias i Pujol University Hospital & Research Institute, Department of Cellular Biology, Physiology & Immunology, Autonomous University of Barcelona, Badalona, Spain, in the analysis Liposome-based immunotherapy against autoimmune diseases: therapeutic effect on multiple sclerosis. Congrats and Thanks.

Summary:

Aim: Based on the ability of apoptosis to induce immunological tolerance, liposomes were generated mimicking apoptotic cells, and they arrest autoimmunity in Type 1 diabetes. Our aim was to validate the immunotherapy in other autoimmune disease: multiple sclerosis. Materials & methods: Phosphatidylserine-rich liposomes were loaded with disease-specific autoantigen. Therapeutic capability of liposomes was assessed in vitro and in vivo. Results: Liposomes induced a tolerogenic phenotype in dendritic cells, and arrested autoimmunity, thus decreasing the incidence, delaying the onset and reducing the severity of experimental disease, correlating with an increase in a probably regulatory CD25+ FoxP3- CD4+ T-cell subset. Conclusion: This is the first work that confirms phosphatidylserine-liposomes as a powerful tool to arrest multiple sclerosis, demonstrating its relevance for clinical application.

Reference:

http://www.futuremedicine.com/doi/full/10.2217/nnm-2016-0410

Product link:

Peptide production Service: http://www.immunostep.com/content/25-peptide-production

CFBlue Annexin V Apoptosis Detection Kit with PI.

An article published this year in “NANOSCALE” using our CFBlue Annexin V Apoptosis Detection Kit with PI, by our customers from Department of Medicine and General Cytometry Service-Nucleus, Cancer Research Centre, (IBMCC/CSIC/USAL/IBSAL), Salamanca, Spain, in the analysis of Functional Insights into the Cellular Response Triggered by Bile-Acid Platinum Compound Conjugated to Biocompatible Ferric Nanoparticles Using Quantitative Proteomic Approaches. Congrats and Thanks.

Summary:

At present, bioferrofluids are employed as multifunctional powerful tools for biomedical applications such as drug delivery, among others. The present study explores the cellular response when bile-acid platinum derivatives are conjugated with bioferrofluids by testing the biological activity in osteosarcoma (MG-63) and T-cell leukemia (Jurkat) cells. The aim of this work is to evaluate the biocompatibility of a bile-acid platinum derivative conjugated with multi-functional polymer coated bioferrofluids by observing the effects on the protein expression profiles and in intracellular pathways of the nanoparticle-stimulated cells. To this end, a mass spectrometry-based approach termed SILAC has been applied to determine in a high-throughput manner the key proteins involved in the cellular respond process (including specific quantitatively identified proteins related to the vesicular transport, cellular structure, cell cycle, biosynthetic process, apoptosis and regulation of the cell cycle). Finally, the biocompatibility was evaluated and validated also by conventional strategies (such as flow cytometry and MTT)

Reference:

http://pubs.rsc.org/en/content/articlehtml/2017/nr/c7nr02196h

Product link:

CFBlue Annexin V Apoptosis Detection Kit with PI: http://www.immunostep.com/apoptosis-tools/3735-anxvkcfb-100t.html

Annexin V binding assay.

An article published this year in “JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH” using our Annexin V binding assay, by our customers from Center for tumor-related epilepsy, Area of Supporting Care, Regina Elena National Cancer Institute, Rome, Italy, in the analysis of In vitro antineoplastic effects of brivaracetam and lacosamide on human glioma cells. Congrats and Thanks.

Summary:

Background: Epilepsy is a frequent symptom in patients with glioma. Although treatment with antiepileptic drugs is generally effective in controlling seizures, drug-resistant patients are not uncommon. Multidrug resistance proteins (MRPs) and P-gp are over-represented in brain tissue of patients with drug-resistant epilepsy, suggesting their involvement in the clearance of antiepileptic medications. In addition to their anticonvulsant action, some drugs have been documented for cytotoxic effects. Aim of this study was to evaluate possible in vitro cytotoxic effects of two new-generation antiepileptic drugs on a human glioma cell line U87MG.

Methods: Cytotoxicity of brivaracetam and lacosamide was tested on U87MG, SW1783 and T98G by MTS assay. Expression of chemoresistance molecules was evaluated using flow cytometry in U87MG and human umbilical vein endothelial cells (HUVECs). To investigate the putative anti-proliferative effect, apoptosis assay, microRNA expression profile and study of cell cycle were performed.

Results: Brivaracetam and lacosamide showed a dose-dependent cytotoxic and anti-migratory effects. Cytotoxicity was not related to apoptosis. The exposure of glioma cells to brivaracetam and lacosamide resulted in the modulation of several microRNAs; particularly, the effect of miR-195-5p modulation seemed to affect cell cycle, while miR-107 seemed to be implicated in the inhibition of cells migration. Moreover, brivaracetam and lacosamide treatment did not modulate the expression of chemoresistance-related molecules MRPs1-3-5, GSTπ, P-gp on U87MG and HUVECs.

Conclusion: Based on antineoplastic effect of brivaracetam and lacosamide on glioma cells, we assume that patients with glioma could benefit by the treatment with these two molecules, in addition to standard therapeutic options.

Reference:

https://jeccr.biomedcentral.com/articles/10.1186/s13046-017-0546-9

Product link:

Annexin V binding assay: http://www.immunostep.com/apoptosis-tools/3731-anxvf-200t.html

CD105 (clon 2H6F1).

An article published this year in “JOURNAL OF CELLULAR PHYSIOLOGY” using our anti Human CD105 (Clon 2H6F11), by our customers from Dipartimento Scienze Cliniche e Molecolari, Clinica di Ematologia, Università Politecnica delle Marche, Ancona, Italy, in the analysis of how Bone marrow adipocytes support haematopoietic stem cell survival. Congrats and Thanks.

Summary:

In bone marrow (BM), haematopoietic elements are mingled with adipocytes (BM-A), which are the most abundant stromal component in the niche. BM-A progressively increase with ageing, eventually occupying up to 50% of BM cavities.

In this work, the role played by BM-A was explored by studying primary human BM-A isolated from hip surgery patients at the molecular level, through microarray analysis, and at the functional level, by assessing their relationship with primary human haematopoietic stem cells (HSC) by the long-term culture initiating cell (LTC-IC) assay.

Findings demonstrated that BM-A are capable of supporting HSC survival in the LTC-IC assay, since after 5 weeks of co-culture, HSC were still able to proliferate and differentiate. Furthermore, critical molecules such as C-X-C motif chemokine 12 (CXCL12), interleukin (IL)-8, colony-stimulating factor 3 (CSF3), and leukaemia inhibitory factor (LIF), were expressed at similar levels in BM-A and in primary human BM mesenchymal stromal cells (BM-MSC), whereas IL-3 was higher in BM-A.

Interestingly, BM-A displayed a different gene expression profile compared with subcutaneous adipose tissue adipocytes (AT-A) collected from abdominal surgery patients, especially in terms of regulation of lipid metabolism, stemness genes and white-to-brown differentiation pathways. Accordingly, analysis of the gene pathways involved in haematopoiesis regulation showed that BM-A are more closely related to BM-MSC than to AT-A.

The present data suggest that BM-A play a supporting role in the haematopoietic niche and directly sustain HSC survival.

Reference:

http://onlinelibrary.wiley.com/doi/10.1002/jcp.26037/full

Product link:

Anti Human CD105 (clon 2H6F1): http://www.immunostep.com/antibodies/2792-cd105.html

FITC Annexin V Apoptosis Detection Kit with PI.

An article published this year in “NUTRIENTS” using our Annexin V-FITC Apoptosis Detection Kit, by our customers from Department of Paediatrics, Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy, in the analysis of Curcumin Anti-Apoptotic Action in a Model of Intestinal Epithelial Inflammatory Damage. Congrats and Thanks.

Summary:

The purpose of this study is to determine if a preventive treatment with curcumin can protect intestinal epithelial cells from inflammatory damage induced by IFNγ. To achieve this goal we have used a human intestinal epithelial cell line (HT29) treated with IFNγ to undergo apoptotic changes that can reproduce the damage of intestinal epithelia exposed to inflammatory cytokines. In this model, we measured the effect of curcumin (curcuminoid from Curcuma Longa) added as a pre-treatment at different time intervals before stimulation with IFNγ. Curcumin administration to HT29 culture before the inflammatory stimulus IFNγ reduced the cell apoptosis rate. This effect gradually declined with the reduction of the curcumin pre-incubation time. This anti-apoptotic action by curcumin pre-treatment was paralleled by a reduction of secreted IL7 in the HT29 culture media, while there was no relevant change in the other cytokine levels. Even though curcumin pre-administration did not impact the activation of the NF-κB pathway, a slight effect on the phosphorylation of proteins in this inflammatory signaling pathway was observed. In conclusion, curcumin pre-treatment can protect intestinal cells from inflammatory damage. These results can be the basis for studying the preventive role of curcumin in inflammatory bowel disease

Reference:

http://www.mdpi.com/2072-6643/9/6/578/html

Product link:

FITC Annexin V Apoptosis Detection Kit with PI: http://www.immunostep.com/apoptosis-tools/3727-anxvkf-100t.html

FITC Annexin V Apoptosis Detection Kit with PI.

An article published this year in “CELL JOURNAL” using our annexin V/PI kit, by our customers from Department of Medical Physics, Iran University of Medical Sciences, and Radiation Biology Research Center, Department of Medical Physics, School of Medicine, Iran University of Medical Sciences, Tehran, Iran, in the analysis of The Role of Radiofrequency Hyperthermia in The Radiosensitization of A Human Prostate Cancer Cell Line. Congrats and Thanks.

Summary:

Objective: This study evaluated enhanced induced DNA damages and apoptosis of a spheroid culture of DU145 prostate cancer cells treated by a combination of radiofrequency hyperthermia (RF HT) with radiation treatment (RT) from an external radiotherapy machine compared to RT alone.

Materials and Methods: In this experimental study, DU145 cells were cultured as spheroids until they reached 300 µm in diameter. We exposed these cultures to either: RF HT for 90 minutes at 43˚C originated from a Celsius TCS system, RF HT followed by RT at doses of 2 Gy or 4 Gy (15 MV energy) with 15-minute interval, or RT alone at the above mentioned doses. The trypan blue exclusion assay, alkaline comet assay, and annexin V/PI flow cytometry were performed to measure cell viability, the amount of DNA damage in an individual cell as the tail moment, and percentage of induced cell apoptosis in response to treatments explained.

Results: We calculated the thermal enhancement factor (TEF) for the combined treatment regime. RF HT followed by the 4 Gy dose of RT resulted in minimum viability (85.33 ± 1.30%), the highest tail moment (1.98 ± 0.18), and highest percentage of apoptotic cells (64.48 ± 3.40%) compared to the other treatments. The results of the TEF assay were 2.54 from the comet assay and 2.33 according to flow cytometry.

Conclusion: The present data suggest that combined treatment of mega voltage X-rays and RF HT can result in significant radiosensitization of prostate cancer cells.

Reference:

http://www.celljournal.org/journal/article/fulltext/the-role-of-radiofrequency-hyperthermia-in-the-radiosensitization-of-human-prostate-cancer-cell-line.html

Product link:

FITC Annexin V Apoptosis Detection Kit with PI: http://www.immunostep.com/apoptosis-tools/3727-anxvkf-100t.html

INTRACELL Kit.

An article published this year in “CELL DEATH AND DISEASE” using our IntraCell Kit, by our customers from Laboratory of Preclinical and Translational Research, IRCCS – Referral Cancer Center of Basilicata (CROB), Rionero in Vulture, Italy, in the analysis of how Knockdown of miR-128a induces Lin28a expression and reverts myeloid differentiation blockage in acute myeloid leukemia. Congrats and Thanks.

Summary:

Lin28A is a highly conserved RNA-binding protein that concurs to control the balance between stemness and differentiation in several tissue lineages. Here, we report the role of miR-128a/Lin28A axis in blocking cell differentiation in acute myeloid leukemia (AML), a genetically heterogeneous disease characterized by abnormally controlled proliferation of myeloid progenitor cells accompanied by partial or total inability to undergo terminal differentiation. First, we found Lin28A underexpressed in blast cells from AML patients and AML cell lines as compared with CD34+ normal precursors. In vitro transfection of Lin28A in NPM1-mutated OCI-AML3 cell line significantly triggered cell-cycle arrest and myeloid differentiation, with increased expression of macrophage associate genes (EGR2, ZFP36 and ANXA1). Furthermore, miR-128a, a negative regulator of Lin28A, was found overexpressed in AML cells compared with normal precursors, especially in acute promyelocytic leukemia (APL) and in ‘AML with maturation’ (according to 2016 WHO classification of myeloid neoplasms and acute leukemia). Its forced overexpression by lentiviral infection in OCI-AML3 downregulated Lin28A with ensuing repression of macrophage-oriented differentiation. Finally, knockdown of miR-128a in OCI-AML3 and in APL/AML leukemic cells (by transfection and lentiviral infection, respectively) induced myeloid cell differentiation and increased expression of Lin28A, EGR2, ZFP36 and ANXA1, reverting myeloid differentiation blockage. In conclusion, our findings revealed a new mechanism for AML differentiation blockage, suggesting new strategies for AML therapy based upon miR-128a inhibition.

Reference:

https://www.nature.com/cddis/journal/v8/n6/full/cddis2017253a.html

Product link:

INTRACELL KIT: http://www.immunostep.com/accesory-reagents/1278-intracell.html