搜索结果: 'methocult media formulations for human hematopoietic cells serum containing'

Fenouille N et al. (DEC 2010) Cancer research 70 23 9659--70

Persistent activation of the Fyn/ERK kinase signaling axis mediates imatinib resistance in chronic myelogenous leukemia cells through upregulation of intracellular SPARC.

SPARC is an extracellular matrix protein that exerts pleiotropic effects on extracellular matrix organization,growth factor availability,cell adhesion,differentiation,and immunity in cancer. Chronic myelogenous leukemia (CML) cells resistant to the BCR-ABL inhibitor imatinib (IM-R cells) were found to overexpress SPARC mRNA. In this study,we show that imatinib triggers SPARC accumulation in a variety of tyrosine kinase inhibitor (TKI)-resistant CML cell lines. SPARC silencing in IM-R cells restored imatinib sensitivity,whereas enforced SPARC expression in imatinib-sensitive cells promoted viability as well as protection against imatinib-mediated apoptosis. Notably,we found that the protective effect of SPARC required intracellular retention inside cells. Accordingly,SPARC was not secreted into the culture medium of IM-R cells. Increased SPARC expression was intimately linked to persistent activation of the Fyn/ERK kinase signaling axis. Pharmacologic inhibition of this pathway or siRNA-mediated knockdown of Fyn kinase resensitized IM-R cells to imatinib. In support of our findings,increased levels of SPARC mRNA were documented in blood cells from CML patients after 1 year of imatinib therapy compared with initial diagnosis. Taken together,our results highlight an important role for the Fyn/ERK signaling pathway in imatinib-resistant cells that is driven by accumulation of intracellular SPARC. View Publication

产品类型：

产品号#：

04100

产品名：

MethoCult™ H4100

1:23

视频

Tools for Breast Cancer Research

发布日期: 01/25/2010

Zhang Q-S et al. (DEC 2010) Blood 116 24 5140--8

Fancd2-/- mice have hematopoietic defects that can be partially corrected by resveratrol.

Progressive bone marrow failure is a major cause of morbidity and mortality in human Fanconi Anemia patients. In an effort to develop a Fanconi Anemia murine model to study bone marrow failure,we found that Fancd2(-/-) mice have readily measurable hematopoietic defects. Fancd2 deficiency was associated with a significant decline in the size of the c-Kit(+)Sca-1(+)Lineage(-) (KSL) pool and reduced stem cell repopulation and spleen colony-forming capacity. Fancd2(-/-) KSL cells showed an abnormal cell cycle status and loss of quiescence. In addition,the supportive function of the marrow microenvironment was compromised in Fancd2(-/-) mice. Treatment with Sirt1-mimetic and the antioxidant drug,resveratrol,maintained Fancd2(-/-) KSL cells in quiescence,improved the marrow microenvironment,partially corrected the abnormal cell cycle status,and significantly improved the spleen colony-forming capacity of Fancd2(-/-) bone marrow cells. We conclude that Fancd2(-/-) mice have readily quantifiable hematopoietic defects,and that this model is well suited for pharmacologic screening studies. View Publication

产品类型：

产品号#：

05350

产品名：

产品手册

Reliable Antibodies for Your Research

产品类型：

品牌：

EasySep

产品号#：

60100

60100.1

60100AD

60100AD.1

60102

60102FI

60104

60104AD

60104AD.1

60104AZ

60104AZ.1

60104BT

60104BT.1

60104BT.2

60104FI

60104FI.1

60104PE

60104PE.1

60106

60106.1

60106AZ

60106AZ.1

60106BT

60106BT.1

60106FI

60106FI.1

60106PE

60106PE.1

60107

60107.1

601

产品名：

抗β-微管蛋白III抗体，克隆AA10

抗β-微管蛋白III抗体，克隆AA10，Alexa Fluor® 488

抗β-微管蛋白III抗体，clone AA10，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3

抗小鼠TCR Gamma/Delta抗体，clone GL3，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3，APC

抗小鼠TCR Gamma/Delta抗体，clone GL3，Biotin

抗小鼠TCR Gamma/Delta抗体，clone GL3，FITC

抗小鼠TCR Gamma/Delta抗体，clone GL3，PE

抗人CD71（转铁蛋白受体）抗体，clone OKT9

抗人CD71（转铁蛋白受体）抗体，clone OKT9，APC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，Biotin

抗人CD71（转铁蛋白受体）抗体，clone OKT9，FITC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，PE

Lidonnici MR et al. (OCT 2010) Cancer research 70 20 7949--59

Expression of the transcriptional repressor Gfi-1 is regulated by C/EBPalpha and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cells.

Ectopic expression of CAAT/enhancer binding protein α (C/EBPα) in p210BCR/ABL-expressing cells induces granulocytic differentiation,inhibits proliferation,and suppresses leukemogenesis. To dissect the molecular mechanisms underlying these biological effects,C/EBPα-regulated genes were identified by microarray analysis in 32D-p210BCR/ABL cells. One of the genes whose expression was activated by C/EBPα in a DNA binding-dependent manner in BCR/ABL-expressing cells is the transcriptional repressor Gfi-1. We show here that C/EBPα interacts with a functional C/EBP binding site in the Gfi-1 5'-flanking region and enhances the promoter activity of Gfi-1. Moreover,in K562 cells,RNA interference-mediated downregulation of Gfi-1 expression partially rescued the proliferation-inhibitory but not the differentiation-inducing effect of C/EBPα. Ectopic expression of wild-type Gfi-1,but not of a transcriptional repressor mutant (Gfi-1P2A),inhibited proliferation and markedly suppressed colony formation but did not induce granulocytic differentiation of BCR/ABL-expressing cells. By contrast,Gfi-1 short hairpin RNA-tranduced CD34(+) chronic myeloid leukemia cells were markedly more clonogenic than the scramble-transduced counterpart. Together,these studies indicate that Gfi-1 is a direct target of C/EBPα required for its proliferation and survival-inhibitory effects in BCR/ABL-expressing cells. View Publication

产品类型：

产品号#：

02690

09600

09650

产品名：

StemSpan™ CC100

StemSpan™ SFEM

Cheng E-C et al. (MAR 2009) Blood 113 12 2826--34

Role for MKL1 in megakaryocytic maturation.

Megakaryoblastic leukemia 1 (MKL1),identified as part of the t(1;22) translocation specific to acute megakaryoblastic leukemia,is highly expressed in differentiated muscle cells and promotes muscle differentiation by activating serum response factor (SRF). Here we show that Mkl1 expression is up-regulated during murine megakaryocytic differentiation and that enforced overexpression of MKL1 enhances megakaryocytic differentiation. When the human erythroleukemia (HEL) cell line is induced to differentiate with 12-O-tetradecanoylphorbol 13-acetate,overexpression of MKL1 results in an increased number of megakaryocytes with a concurrent increase in ploidy. MKL1 overexpression also promotes megakaryocytic differentiation of primary human CD34(+) cells cultured in the presence of thrombopoietin. The effect of MKL1 is abrogated when SRF is knocked down,suggesting that MKL1 acts through SRF. Consistent with these findings in human cells,knockout of Mkl1 in mice leads to reduced platelet counts in peripheral blood,and reduced ploidy in bone marrow megakaryocytes. In conclusion,MKL1 promotes physiologic maturation of human and murine megakaryocytes. View Publication

产品类型：

产品号#：

09500

09600

09650

04960

04902

04900

04963

04962

04970

04971

04901

产品名：

BIT 9500血清替代物

StemSpan™ SFEM

MegaCult™-C胶原和无细胞因子培养基

胶原蛋白溶液

MegaCult™-C无细胞因子培养基

双室载玻片套件

MegaCult™-C CFU-Mk染色试剂盒

MegaCult™-C无细胞因子全套试剂盒

MegaCult™-C含细胞因子全套试剂盒

MegaCult™-C含细胞因子培养基

Ló et al. (NOV 2009) Cancer immunology,immunotherapy : CII 58 11 1853--64

Role of polymorphic Fc gamma receptor IIIa and EGFR expression level in cetuximab mediated, NK cell dependent in vitro cytotoxicity of head and neck squamous cell carcinoma cells.

Immunotherapy with the EGFR-specific mAb cetuximab is clinically effective in 10-20% of patients with squamous cell carcinoma of the head and neck (SCCHN). Little information is available about the mechanism(s) underlying patients' differential clinical response to cetuximab-based immunotherapy,although this information may contribute to optimizing the design of cetuximab-based immunotherapy. Our understanding of these mechanisms would benefit from the characterization of the variables which influence the extent of cell dependent-lysis of SCCHN cells incubated with cetuximab in vitro. Therefore,in this study we have investigated the role of FcgammaR IIIa-158 genotype expressed by effector NK cells,cetuximab concentration,and EGFR expression level by SCCHN cells in the extent of their in vitro lysis and in the degree of NK cell activation. PBMC or purified CD56+ NK cells genotyped at IIIa codon 158 and SCCHN cell lines expressing different levels of EGFR have been used as effectors and targets,respectively,in antibody dependent cellular cytotoxicity (ADCC) assays. Furthermore,supernatants from ADCC assays were analyzed for cytokine and chemokine levels using multiplexed ELISA. We found that the extent of lysis of SCCHN cells was influenced by the EGFR expression level,cetuximab concentration,and FcgammaR polymorphism. Effector cells expressing the FcgammaR IIIa-158 VV allele were significantly (P textless 0.0001) more effective than those expressing FcgammaR IIIa VF and FF [corrected] alleles in mediating lysis of SCCHN cells expressed higher levels of the activation markers CD69 and CD107a,and secreted significantly (P textless 0.05) larger amounts of inflammatory cytokines and chemokines. IL-2 or IL-15 treatment increased cetuximab-mediated ADCC by poor binding FcgammaR IIIa 158 FF expressing NK cells. The importance of the FcgammaR IIIa-158 polymorphism in cytotoxicity of SCCHN cells by NK cells supports a potential role for immune activation and may explain patient variability of cetuximab mediated clinical responses. Cellular and secreted immune profiles and FcgammaR genotypes from patients' lymphocytes may provide clinically useful biomarkers of immune activation in cetuximab treated patients. View Publication

产品类型：

产品号#：

19055

19055RF

产品名：

EasySep™人NK细胞富集试剂盒

RoboSep™ 人NK细胞富集试剂盒含滤芯吸头

Jing J et al. ( 2012) Molecular cancer therapeutics 11 3 720--729

Comprehensive predictive biomarker analysis for MEK inhibitor GSK1120212.

The MEK1 and MEK2 inhibitor GSK1120212 is currently in phase II/III clinical development. To identify predictive biomarkers,sensitivity to GSK1120212 was profiled for 218 solid tumor cell lines and 81 hematologic malignancy cell lines. For solid tumors,RAF/RAS mutation was a strong predictor of sensitivity. Among RAF/RAS mutant lines,co-occurring PIK3CA/PTEN mutations conferred a cytostatic response instead of a cytotoxic response for colon cancer cells that have the biggest representation of the comutations. Among KRAS mutant cell lines,transcriptomics analysis showed that cell lines with an expression pattern suggestive of epithelial-to-mesenchymal transition were less sensitive to GSK1120212. In addition,a proportion of cell lines from certain tissue types not known to carry frequent RAF/RAS mutations also seemed to be sensitive to GSK1120212. Among these were breast cancer cell lines,with triple negative breast cancer cell lines being more sensitive than cell lines from other breast cancer subtypes. We identified a single gene DUSP6,whose expression was associated with sensitivity to GSK1120212 and lack of expression associated with resistance irrelevant of RAF/RAS status. Among hematologic cell lines,acute myeloid leukemia and chronic myeloid leukemia cell lines were particularly sensitive. Overall,this comprehensive predictive biomarker analysis identified additional efficacy biomarkers for GSK1120212 in RAF/RAS mutant solid tumors and expanded the indication for GSK1120212 to patients who could benefit from this therapy despite the RAF/RAS wild-type status of their tumors. View Publication

产品类型：

产品号#：

73502

73504

产品名：

Druker BJ (DEC 2008) Blood 112 13 4808--17

Translation of the Philadelphia chromosome into therapy for CML.

Throughout its history,chronic myeloid leukemia (CML) has set precedents for cancer research and therapy. These range from the identification of the first specific chromosomal abnormality associated with cancer to the development of imatinib as a specific,targeted therapy for the disease. The successful development of imatinib as a therapeutic agent for CML can be attributed directly to decades of scientific discoveries. These discoveries determined that the BCR-ABL tyrosine kinase is the critical pathogenetic event in CML and an ideal target for therapy. This was confirmed in clinical trials of imatinib,with imatinib significantly improving the long-term survival of patients with CML. Continuing in this tradition of scientific discoveries leading to improved therapies,the understanding of resistance to imatinib has rapidly led to strategies to circumvent resistance. Continued studies of hematologic malignancies will allow this paradigm of targeting molecular pathogenetic events to be applied to many additional hematologic cancers. View Publication

产品类型：

产品号#：

72532

72534

产品名：

Imatinib (Mesylate)

Imatinib (Mesylate), 100 mg

How to Process a Leukopak for Downstream Cell Isolation

13:43

视频

How to Process a Leukopak for Downstream Cell Isolation

发布日期: 02/16/2022

High-Throughput Isolation of Extracellular Vesicles for Next-Generation Diagnostic Assays

25:25

线上讲座

High-Throughput Isolation of Extracellular Vesicles for Next-Generation Diagnostic Assays

发布日期: 11/14/2023

产品手册

NeuroCult™: Reagents for Brain Tumor Stem Cell Research

产品类型：

品牌：

NeuroCult

产品号#：

01700

01705

01701

01702

05700

05702

05704

05707

05715

05740

05742

05751

05752

05761

05771

05772

07920

产品名：

ALDEFLUOR™ 试剂盒

ALDEFLUOR™ DEAB试剂, 1.5 mM, 1 mL

ALDEFLUOR™检测缓冲液

NeuroCult™ 基础培养基（小鼠和大鼠）

NeuroCult™扩增试剂盒（小鼠和大鼠）

NeuroCult™ 分化试剂盒（小鼠和大鼠）

NeuroCult™化学解离试剂盒（小鼠）

NeuroCult™成年中枢神经系统（CNS）组织酶解试剂盒（小鼠和大鼠）

NeuroCult™ NS-A 扩增试剂盒（人）

NeuroCult™ NS-A 分化试剂盒（人）

用于小鼠和大鼠神经干细胞和祖细胞分化培养的试剂盒

ACCUTASE™

搜索结果: 'methocult media formulations for human hematopoietic cells serum containing'

Persistent activation of the Fyn/ERK kinase signaling axis mediates imatinib resistance in chronic myelogenous leukemia cells through upregulation of intracellular SPARC.

Fancd2-/- mice have hematopoietic defects that can be partially corrected by resveratrol.

Expression of the transcriptional repressor Gfi-1 is regulated by C/EBPalpha and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cells.

Role for MKL1 in megakaryocytic maturation.

Role of polymorphic Fc gamma receptor IIIa and EGFR expression level in cetuximab mediated, NK cell dependent in vitro cytotoxicity of head and neck squamous cell carcinoma cells.

Comprehensive predictive biomarker analysis for MEK inhibitor GSK1120212.

Translation of the Philadelphia chromosome into therapy for CML.

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