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

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

60104

60104AD.1

60104AZ

60104AZ.1

60104BT

60104BT.1

60104FI.1

60104PE

60104PE.1

60106

60106.1

60106AZ

60106AZ.1

60106BT

60106FI

60106FI.1

60106PE

60106PE.1

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

Yamamizu K et al. (DEC 2013) Stem Cell Reports 1 6 545--559

Identification of Transcription Factors for Lineage-Specific ESC Differentiation

A network of transcription factors (TFs) determines cell identity,but identity can be altered by overexpressing a combination of TFs. However,choosing and verifying combinations of TFs for specific cell differentiation have been daunting due to the large number of possible combinations of 2,000 TFs. Here,we report the identification of individual TFs for lineage-specific cell differentiation based on the correlation matrix of global gene expression profiles. The overexpression of identified TFs-Myod1,Mef2c,Esx1,Foxa1,Hnf4a,Gata2,Gata3,Myc,Elf5,Irf2,Elf1,Sfpi1,Ets1,Smad7,Nr2f1,Sox11,Dmrt1,Sox9,Foxg1,Sox2,or Ascl1-can direct efficient,specific,and rapid differentiation into myocytes,hepatocytes,blood cells,and neurons. Furthermore,transfection of synthetic mRNAs of TFs generates their appropriate target cells. These results demonstrate both the utility of this approach to identify potent TFs for cell differentiation,and the unanticipated capacity of single TFs directly guides differentiation to specific lineage fates. View Publication

产品类型：

产品号#：

05700

05704

产品名：

NeuroCult™ 基础培养基(小鼠&大鼠)

NeuroCult™ 分化试剂盒 (小鼠&大鼠)

Lee SB et al. (JAN 2016) Nature 529 7585 172--7

An ID2-dependent mechanism for VHL inactivation in cancer.

Mechanisms that maintain cancer stem cells are crucial to tumour progression. The ID2 protein supports cancer hallmarks including the cancer stem cell state. HIFα transcription factors,most notably HIF2α (also known as EPAS1),are expressed in and required for maintenance of cancer stem cells (CSCs). However,the pathways that are engaged by ID2 or drive HIF2α accumulation in CSCs have remained unclear. Here we report that DYRK1A and DYRK1B kinases phosphorylate ID2 on threonine 27 (Thr27). Hypoxia downregulates this phosphorylation via inactivation of DYRK1A and DYRK1B. The activity of these kinases is stimulated in normoxia by the oxygen-sensing prolyl hydroxylase PHD1 (also known as EGLN2). ID2 binds to the VHL ubiquitin ligase complex,displaces VHL-associated Cullin 2,and impairs HIF2α ubiquitylation and degradation. Phosphorylation of Thr27 of ID2 by DYRK1 blocks ID2-VHL interaction and preserves HIF2α ubiquitylation. In glioblastoma,ID2 positively modulates HIF2α activity. Conversely,elevated expression of DYRK1 phosphorylates Thr27 of ID2,leading to HIF2α destabilization,loss of glioma stemness,inhibition of tumour growth,and a more favourable outcome for patients with glioblastoma. View Publication

产品类型：

产品号#：

05700

05701

05702

产品名：

NeuroCult™ 基础培养基(小鼠&大鼠)

NeuroCult™ 扩增添加物 (小鼠&大鼠)

NeuroCult™ 扩增试剂盒 (小鼠&大鼠)

Rahman M et al. (SEP 2013) Future Oncology 9 9 1389--1396

Controlling tumor invasion: bevacizumab and BMP4 for glioblastoma

AIM Bevacizumab has been reported to result in increased tumor invasion when used to treat malignant glioma. We hypothesized that BMP4 would prevent diffuse tumor infiltration induced by bevacizumab for malignant glioma in a xenograft model. METHODS Human glioblastoma (GBM) tumor cells were implanted in the striatum of immunocompromised mice. The animals were treated with bevacizumab and BMP4. Tumor growth and invasion were measured. RESULTS The bevacizumab-treated mice had increased survival compared with control animals (p = 0.02). BMP4 alone did not result in improved survival (p = 1.0). The bevacizumab (p = 0.006) and bevacizumab plus BMP4 (p = 0.006) groups demonstrated significantly decreased total tumor size compared with control. Tumor invasion was significantly decreased in the bevacizumab (p = 0.005),BMP4 (p = 0.04) alone and bevacizumab plus BMP4 (p = 0.002) groups compared with control. No synergistic effect between bevacizumab and BMP4 was observed. CONCLUSION Bevacizumab treatment did not result in diffuse infiltration of human GBM in a mouse xenograft model. BMP4 did have an independent favorable effect on GBM that was not synergistic with bevacizumab treatment. View Publication

产品类型：

产品号#：

05750

05751

产品名：

NeuroCult™ NS-A 基础培养基（人）

NeuroCult™ NS-A 扩增试剂盒（人）

Virtual STEMCELL Seminar: Organoids as Models for Cerebellar Development

17:27

线上讲座

Virtual STEMCELL Seminar: Organoids as Models for Cerebellar Development

发布日期: 07/09/2020

Propel Your Neural Research—with a Workflow Designed for Discovery

2:33

视频

Propel Your Neural Research—with a Workflow Designed for Discovery

发布日期: 12/01/2025

产品手册

NeuroCult™: Reagents for Brain Tumor Stem Cell Research

产品类型：

品牌：

NeuroCult

产品号#：

01700

01702

01705

05700

05702

05704

05707

05715

05751

05752

05761

07920

产品名：

ALDEFLUOR™ 试剂盒

ALDEFLUOR™测定缓冲液

ALDEFLUOR™ DEAB试剂

NeuroCult™ 基础培养基(小鼠&大鼠)

NeuroCult™ 扩增试剂盒 (小鼠&大鼠)

NeuroCult™ 分化试剂盒 (小鼠&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™

Er JC et al. (FEB 2015) Angewandte Chemie - International Edition 54 8 2442--2446

Neuo: A fluorescent chemical probe for live neuron labeling

To address existing limitations in live neuron imaging,we have developed NeuO,a novel cell-permeable fluorescent probe with an unprecedented ability to label and image live neurons selectively over other cells in the brain. NeuO enables robust live neuron imaging and isolation in vivo and in vitro across species; its versatility and ease of use sets the basis for its development in a myriad of neuronal targeting applications. View Publication

产品类型：

产品号#：

01801

产品名：

NeuroFluor™NeuO

Chakrabarti L et al. (JAN 2012) Frontiers in oncology 2 82

Reversible adaptive plasticity: a mechanism for neuroblastoma cell heterogeneity and chemo-resistance.

We describe a novel form of tumor cell plasticity characterized by reversible adaptive plasticity in murine and human neuroblastoma. Two cellular phenotypes were defined by their ability to exhibit adhered,anchorage dependent (AD) or sphere forming,anchorage independent (AI) growth. The tumor cells could transition back and forth between the two phenotypes and the transition was dependent on the culture conditions. Both cell phenotypes exhibited stem-like features such as expression of nestin,self-renewal capacity,and mesenchymal differentiation potential. The AI tumorspheres were found to be more resistant to chemotherapy and proliferated slower in vitro compared to the AD cells. Identification of specific molecular markers like MAP2,β-catenin,and PDGFRβ enabled us to characterize and observe both phenotypes in established mouse tumors. Irrespective of the phenotype originally implanted in mice,tumors grown in vivo show phenotypic heterogeneity in molecular marker signatures and are indistinguishable in growth or histologic appearance. Similar molecular marker heterogeneity was demonstrated in primary human tumor specimens. Chemotherapy or growth factor receptor inhibition slowed tumor growth in mice and promoted initial loss of AD or AI heterogeneity,respectively. Simultaneous targeting of both phenotypes led to further tumor growth delay with emergence of new unique phenotypes. Our results demonstrate that neuroblastoma cells are plastic,dynamic,and may optimize their ability to survive by changing their phenotype. Phenotypic switching appears to be an adaptive mechanism to unfavorable selection pressure and could explain the phenotypic and functional heterogeneity of neuroblastoma. View Publication

产品类型：

产品号#：

05700

05701

05702

产品名：

NeuroCult™ 基础培养基(小鼠&大鼠)

NeuroCult™ 扩增添加物 (小鼠&大鼠)

NeuroCult™ 扩增试剂盒 (小鼠&大鼠)

Di Cristofori A et al. (JUL 2015) Oncotarget 6 19 17514--31

The vacuolar H+ ATPase is a novel therapeutic target for glioblastoma.

The vacuolar H+ ATPase (V-ATPase) is a proton pump responsible for acidification of cellular microenvironments,an activity exploited by tumors to survive,proliferate and resist to therapy. Despite few observations,the role of V-ATPase in human tumorigenesis remains unclear.We investigated the expression of ATP6V0C,ATP6V0A2,encoding two subunits belonging to the V-ATPase V0 sector and ATP6V1C,ATP6V1G1,ATPT6V1G2,ATP6V1G3,which are part of the V1 sector,in series of adult gliomas and in cancer stem cell-enriched neurospheres isolated from glioblastoma (GBM) patients. ATP6V1G1 expression resulted significantly upregulated in tissues of patients with GBM and correlated with shorter patients' overall survival independent of clinical variables.ATP6V1G1 knockdown in GBM neurospheres hampered sphere-forming ability,induced cell death,and decreased matrix invasion,a phenotype not observed in GBM monolayer cultures. Treating GBM organotypic cultures or neurospheres with the selective V-ATPase inhibitor bafilomycin A1 reproduced the effects of ATP6V1G1 siRNA and strongly suppressed expression of the stem cell markers Nestin,CD133 and transcription factors SALL2 and POU3F2 in neurospheres.These data point to ATP6V1G1 as a novel marker of poor prognosis in GBM patients and identify V-ATPase inhibition as an innovative therapeutic strategy for GBM. View Publication

产品类型：

产品号#：

05750

05751

产品名：

NeuroCult™ NS-A 基础培养基（人）

NeuroCult™ NS-A 扩增试剂盒（人）

Villa GR et al. (NOV 2016) Cancer cell 30 5 683--693

An LXR-Cholesterol Axis Creates a Metabolic Co-Dependency for Brain Cancers.

Small-molecule inhibitors targeting growth factor receptors have failed to show efficacy for brain cancers,potentially due to their inability to achieve sufficient drug levels in the CNS. Targeting non-oncogene tumor co-dependencies provides an alternative approach,particularly if drugs with high brain penetration can be identified. Here we demonstrate that the highly lethal brain cancer glioblastoma (GBM) is remarkably dependent on cholesterol for survival,rendering these tumors sensitive to Liver X receptor (LXR) agonist-dependent cell death. We show that LXR-623,a clinically viable,highly brain-penetrant LXRα-partial/LXRβ-full agonist selectively kills GBM cells in an LXRβ- and cholesterol-dependent fashion,causing tumor regression and prolonged survival in mouse models. Thus,a metabolic co-dependency provides a pharmacological means to kill growth factor-activated cancers in the CNS. View Publication

产品类型：

产品号#：

05750

05751

产品名：

NeuroCult™ NS-A 基础培养基（人）

NeuroCult™ NS-A 扩增试剂盒（人）

An MC et al. ( 2014) PLoS currents 6 1--19

Polyglutamine Disease Modeling: Epitope Based Screen for Homologous Recombination using CRISPR/Cas9 System.

We have previously reported the genetic correction of Huntington's disease (HD) patient-derived induced pluripotent stem cells using traditional homologous recombination (HR) approaches. To extend this work,we have adopted a CRISPR-based genome editing approach to improve the efficiency of recombination in order to generate allelic isogenic HD models in human cells. Incorporation of a rapid antibody-based screening approach to measure recombination provides a powerful method to determine relative efficiency of genome editing for modeling polyglutamine diseases or understanding factors that modulate CRISPR/Cas9 HR. View Publication

产品类型：

产品号#：

85850

85857

产品名：

mTeSR™1

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

Identification of Transcription Factors for Lineage-Specific ESC Differentiation

An ID2-dependent mechanism for VHL inactivation in cancer.

Controlling tumor invasion: bevacizumab and BMP4 for glioblastoma

Neuo: A fluorescent chemical probe for live neuron labeling

Reversible adaptive plasticity: a mechanism for neuroblastoma cell heterogeneity and chemo-resistance.

The vacuolar H+ ATPase is a novel therapeutic target for glioblastoma.

An LXR-Cholesterol Axis Creates a Metabolic Co-Dependency for Brain Cancers.

Polyglutamine Disease Modeling: Epitope Based Screen for Homologous Recombination using CRISPR/Cas9 System.

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