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

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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

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HLA Antibodies for Purity Assessment

产品类型：

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EasySep

产品号#：

15276

15664HLA

15684HLA

60018

60018AD

60018AD.1

60018AZ

60018AZ.1

60018BT

60018BT.1

60018FI

60018FI.1

60018PE

60018PE.1

60018PS

60018PS.1

60018PB

60018PB.1

60018PB.2

60022

60022AZ

60022AZ.1

60022BT

60022BT.1

60022FI

60022FI.1

60022PE

60022PE.1

60022PS

600

产品名：

RosetteSep™人脐带血祖细胞完全富集试剂盒

RosetteSep™ HLA粒细胞去除抗体混合物

抗人CD45抗体, 克隆号HI30

抗人CD45抗体，clone HI30，Alexa Fluor® 488

抗人CD45抗体，克隆HI30，Alexa Fluor® 488

抗人CD45抗体，克隆HI30，APC

抗人CD45抗体，克隆HI30，Biotin

抗人CD45抗体，克隆HI30，FITC

抗人CD45抗体，克隆HI30，PE

抗人CD45抗体，克隆HI30，PerCP-Cy5.5

抗人CD45抗体，克隆HI30，Pacific Blue™

抗人CD8a抗体，克隆RPA-T8

抗人CD8a抗体，克隆RPA-T8，APC

抗人CD8a抗体，clone RPA-T8，APC

抗人CD8a抗体，克隆RPA-T8，FITC

抗人CD8a抗体，克隆RPA-T8，PE

抗人CD8a抗体，克隆RPA-T8，PerCP-Cy5.5

Event

Association for Molecular Pathology (AMP)

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产品名：

Organoid-Based Assays for Disease Modeling

24:55

线上讲座

Organoid-Based Assays for Disease Modeling

发布日期: 11/30/22

Kortylewski M et al. (DEC 2005) Nature medicine 11 12 1314--21

Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity.

The immune system can act as an extrinsic suppressor of tumors. Therefore,tumor progression depends in part on mechanisms that downmodulate intrinsic immune surveillance. Identifying these inhibitory pathways may provide promising targets to enhance antitumor immunity. Here,we show that Stat3 is constitutively activated in diverse tumor-infiltrating immune cells,and ablating Stat3 in hematopoietic cells triggers an intrinsic immune-surveillance system that inhibits tumor growth and metastasis. We observed a markedly enhanced function of dendritic cells,T cells,natural killer (NK) cells and neutrophils in tumor-bearing mice with Stat3(-/-) hematopoietic cells,and showed that tumor regression requires immune cells. Targeting Stat3 with a small-molecule drug induces T cell- and NK cell-dependent growth inhibition of established tumors otherwise resistant to direct killing by the inhibitor. Our findings show that Stat3 signaling restrains natural tumor immune surveillance and that inhibiting hematopoietic Stat3 in tumor-bearing hosts elicits multicomponent therapeutic antitumor immunity. View Publication

产品类型：

产品号#：

18709

18709RF

产品名：

EasySep™小鼠定制正选试剂盒

RoboSep™ 小鼠定制正选试剂盒含滤芯吸头

Nemeth MJ et al. (SEP 2006) Proceedings of the National Academy of Sciences of the United States of America 103 37 13783--8

Hmgb3 regulates the balance between hematopoietic stem cell self-renewal and differentiation.

Hmgb3 is an X-linked member of a family of sequence-independent chromatin-binding proteins that is preferentially expressed in hematopoietic stem cells (HSC). Hmgb3-deficient mice (Hmgb3(-/Y)) contain normal numbers of HSCs,capable of self-renewal and hematopoietic repopulation,but fewer common lymphoid (CLP) and common myeloid progenitors (CMP). In this study,we tested the hypothesis that Hmgb3(-/Y) HSCs are biased toward self-renewal at the expense of progenitor production. Wild-type and Hmgb3(-/Y) CLPs and CMPs proliferate and differentiate equally in vitro,indicating that CLP and CMP function normally in Hmgb3(-/Y) mice. Hmgb3(-/Y) HSCs exhibit constitutive activation of the canonical Wnt signaling pathway,which regulates stem cell self-renewal. Increased Wnt signaling in Hmgb3(-/Y) HSCs corresponds to increased expression of Dvl1,a positive regulator of the canonical Wnt pathway. To induce hematopoietic stress and a subsequent response from HSCs,we treated Hmgb3(-/Y) mice with 5-fluorouracil. Hmgb3(-/Y) mice exhibit a faster recovery of functional HSCs after administration of 5-fluorouracil compared with wild-type mice,which may be due to the increased Wnt signaling. Furthermore,the recovery of HSC number in Hmgb3(-/Y) mice occurs more rapidly than CLP and CMP recovery. From these data,we propose a model in which Hmgb3 is required for the proper balance between HSC self-renewal and differentiation. View Publication

产品类型：

产品号#：

03630

03434

03444

09600

09650

产品名：

MethoCult™M3630

MethoCult™GF M3434

StemSpan™ SFEM

M. Romera-Hern\'andez et al. (jun 2019) Current protocols in immunology 125 1 e73

Identification of Group 2 Innate Lymphoid Cells in Mouse Lung, Liver, Small Intestine, Bone Marrow, and Mediastinal and Mesenteric Lymph Nodes.

Innate lymphoid cells (ILCs) are a heterogeneous family of lymphocytes that populate barrier and non-barrier tissues. ILCs regulate immune responses to pathogens and commensals but also sustain metabolic homeostasis,tissue remodeling after injury and establish dialogue with the nervous system. ILCs rapidly become activated in the absence of adaptive antigen receptors by responding to signaling molecules provided by hematopoietic or non-hematopoietic cells. Here we provide protocols designed for processing the lung,liver,small intestine,bone marrow,mediastinal and mesenteric lymph nodes in order to obtain a purified leukocyte fraction of cells,in which ILC2 enrichment is optimized. In addition,we describe in detail the methodologies used to activate ILC2s and the assays necessary for the detection of their effector cytokines. We highlight the differences in ILC2 characterization within distinct tissues that we have recently identified. {\textcopyright} 2019 by John Wiley Sons,Inc. View Publication

产品类型：

产品号#：

19842

产品名：

EasySep™小鼠ILC2富集试剂盒

Prabhu VV et al. (APR 2016) Cancer research 76 7 1989--1999

Small-Molecule Prodigiosin Restores p53 Tumor Suppressor Activity in Chemoresistant Colorectal Cancer Stem Cells via c-Jun-Mediated &dollar;&dollar;Np73 Inhibition and p73 Activation.

Tumor suppressor p53 is frequently mutated or inactivated in colorectal cancer. In contrast,p53 family member p73 is rarely mutated in colorectal cancer and p73 activation elicits p53-like tumor suppression. Colorectal cancer stem cells (CRCSC) comprise a rare self-renewing subpopulation that contributes to tumor maintenance and chemoresistance. p53 restoration is known to target CRCSCs,but p73 restoration in CRCSCs has not been examined. In this study,we investigated the effects of the small-molecule prodigiosin,which restores the p53 pathway in tumor cells via p73 activation,on CRCSCs in vitro and in vivo Prodigiosin prevented colonosphere formation independent of p53 status and reduced the viability of self-renewing,5-fluorouracil-resistant Aldefluor positive [Aldefluor(+)] CRCSCs in vitro Furthermore,prodigiosin inhibited the growth of xenograft tumors initiated with Aldefluor+ cells without toxic effects and limited the tumorigenic potential of these cells. Consistently,prodigiosin induced activation of a p53-responsive luciferase reporter in colonospheres,Aldefluor(+) cells,and tumor xenografts. Mechanistic studies revealed that prodigiosin increased the levels of p73 and reduced levels of the oncogenic N-terminally truncated isoform $$Np73 in Aldefluor(+) cells. Accordingly,p73 knockdown or $$Np73 overexpression suppressed prodigiosin-mediated inhibition of colonosphere formation. Moreover,prodigiosin increased levels of the transcription factor c-Jun,a regulator of p73 and $$Np73,in both the cytoplasm and nucleus. c-Jun knockdown attenuated prodigiosin-mediated p53-reporter activation,$$Np73 downregulation,p73 activation,and cell death. Collectively,our findings highlight the previously uncharacterized use of p73-activating therapeutics to target CRCSCs. Cancer Res; 76(7); 1989-99. textcopyright2016 AACR. View Publication

产品类型：

产品号#：

05620

产品名：

MammoCult™人培养基试剂盒

Donahue RE et al. (JAN 2000) Blood 95 2 445--52

High levels of lymphoid expression of enhanced green fluorescent protein in nonhuman primates transplanted with cytokine-mobilized peripheral blood CD34(+) cells.

We have used a murine retrovirus vector containing an enhanced green fluorescent protein complimentary DNA (EGFP cDNA) to dynamically follow vector-expressing cells in the peripheral blood (PB) of transplanted rhesus macaques. Cytokine mobilized CD34(+) cells were transduced with an amphotropic vector that expressed EGFP and a dihydrofolate reductase cDNA under control of the murine stem cell virus promoter. The transduction protocol used the CH-296 recombinant human fibronectin fragment and relatively high concentrations of the flt-3 ligand and stem cell factor. Following transplantation of the transduced cells,up to 55% EGFP-expressing granulocytes were obtained in the peripheral circulation during the early posttransplant period. This level of myeloid marking,however,decreased to 0.1% or lower within 2 weeks. In contrast,EGFP expression in PB lymphocytes rose from 2%-5% shortly following transplantation to 10% or greater by week 5. After 10 weeks,the level of expression in PB lymphocytes continued to remain at 3%-5% as measured by both flow cytometry and Southern blot analysis,and EGFP expression was observed in CD4(+),CD8(+),CD20(+),and CD16/56(+) lymphocyte subsets. EGFP expression was only transiently detected in red blood cells and platelets soon after transplantation. Such sustained levels of lymphocyte marking may be therapeutic in a number of human gene therapy applications that require targeting of the lymphoid compartment. The transient appearance of EGFP(+) myeloid cells suggests that transduction of a lineage-restricted myeloid progenitor capable of short-term engraftment was obtained with this protocol. (Blood. 2000;95:445-452) View Publication

产品类型：

产品号#：

04436

04064

04100

04230

04236

04431

04434

04444

04464

04531

04535

04545

04536

04564

04035

04330

04034

04044

04435

04445

04534

04544

产品名：

MethoCult™ SF H4436

MethoCult™ H4034 Optimum启动试剂盒套装

MethoCult™ H4100

MethoCult™H4230

MethoCult™SF H4236

MethoCult™H4431

MethoCult™H4434经典

MethoCult™ H4434 Classic启动试剂盒套装

MethoCult™H4531

MethoCult™H4535富集无EPO

MethoCult™ H4535 Enriched，不含EPO

MethoCult™ SF H4536

入门套件MethoCult™H4534经典无EPO

MethoCult™H4035 Optimum无EPO

MethoCult™H4330

MethoCult™H4034 Optimum

MethoCult™H4435富集

MethoCult™H4534经典无EPO

Liu B et al. (MAR 2014) PLoS ONE 9 3 e90615

Nanog1 in NTERA-2 and recombinant NanogP8 from somatic cancer cells adopt multiple protein conformations and migrate at multiple M.W species

Human Nanog1 is a 305-amino acid (aa) homeodomain-containing transcription factor critical for the pluripotency of embryonic stem (ES) and embryonal carcinoma (EC) cells. Somatic cancer cells predominantly express a retrogene homolog of Nanog1 called NanogP8,which is ˜99% similar to Nanog at the aa level. Although the predicted M.W of Nanog1/NanogP8 is ∼35 kD,both have been reported to migrate,on Western blotting (WB),at apparent molecular masses of 29-80 kD. Whether all these reported protein bands represent authentic Nanog proteins is unclear. Furthermore,detailed biochemical studies on Nanog1/NanogpP8 have been lacking. By combining WB using 8 anti-Nanog1 antibodies,immunoprecipitation,mass spectrometry,and studies using recombinant proteins,here we provide direct evidence that the Nanog1 protein in NTERA-2 EC cells exists as multiple M.W species from ˜22 kD to 100 kD with a major 42 kD band detectable on WB. We then demonstrate that recombinant NanogP8 (rNanogP8) proteins made in bacteria using cDNAs from multiple cancer cells also migrate,on denaturing SDS-PAGE,at ˜28 kD to 180 kD. Interestingly,different anti-Nanog1 antibodies exhibit differential reactivity towards rNanogP8 proteins,which can spontaneously form high M.W protein species. Finally,we show that most long-term cultured cancer cell lines seem to express very low levels of or different endogenous NanogP8 protein that cannot be readily detected by immunoprecipitation. Altogether,the current study reveals unique biochemical properties of Nanog1 in EC cells and NanogP8 in somatic cancer cells. View Publication

产品类型：

产品号#：

05850

05857

05870

05875

85850

85857

85870

85875

产品名：

mTeSR™1

A. Ferrelli et al. (Aug 2025) HemaSphere 9 8

Mesenchymal stromal cells from JAK2 V617F myeloproliferative neoplasms support healthy and malignant hematopoiesis in a humanized scaffold model in vivo

Myeloproliferative Neoplasms (MPN) are malignancies of hematopoietic stem and progenitor cells (HSPCs) that lead to the overproduction of mature blood cells. These disorders include Essential Thrombocythemia (ET),Polycythemia Vera (PV),and Primary Myelofibrosis (PMF),primarily driven by somatic mutations such as JAK2 V617F . Research indicates that mesenchymal stromal cells (MSCs) support fibrosis in PMF,though their role in ET and PV remains less clear. Furthermore,in vivo studies of ET/PV HSPCs remain a challenge due to low engraftment levels in xenograft models. We employed a 3D scaffold model to create an MPN humanized xenograft mouse model,enabling in vivo functional studies of primary MPN progenitor cells and the supportive role of human MSCs. Using this model,we first demonstrated robust hematopoietic support of healthy (HD) HSPCs by PV and ET MSCs. We then investigated the role of MSCs in sustaining JAK2 V617F mutant cells by using a CRISPR‐Cas9 editing model,along with primary PV and ET HSPCs. Our results showed consistent engraftment of CRISPR‐edited JAK2 V617F mutant HSPCs and PV and ET patient‐derived HSPCs in scaffolds seeded with HD,PV,and ET stroma,providing the first in vivo evidence that PV and ET MSCs can sustain both healthy and MPN‐associated hematopoiesis. Furthermore,HD MSCs were also capable of sustaining PV and ET HSPCs in vivo. Overall,we present the first humanized MPN xenograft model that offers valuable insights into how human BM MSCs interact with JAK2 V617F mutant clones. View Publication

产品类型：

产品号#：

05150

产品名：

MyeloCult™H5100

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

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

Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity.

Hmgb3 regulates the balance between hematopoietic stem cell self-renewal and differentiation.

Identification of Group 2 Innate Lymphoid Cells in Mouse Lung, Liver, Small Intestine, Bone Marrow, and Mediastinal and Mesenteric Lymph Nodes.

Small-Molecule Prodigiosin Restores p53 Tumor Suppressor Activity in Chemoresistant Colorectal Cancer Stem Cells via c-Jun-Mediated &dollar;&dollar;Np73 Inhibition and p73 Activation.

High levels of lymphoid expression of enhanced green fluorescent protein in nonhuman primates transplanted with cytokine-mobilized peripheral blood CD34(+) cells.

Nanog1 in NTERA-2 and recombinant NanogP8 from somatic cancer cells adopt multiple protein conformations and migrate at multiple M.W species

Mesenchymal stromal cells from JAK2 V617F myeloproliferative neoplasms support healthy and malignant hematopoiesis in a humanized scaffold model in vivo

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

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