搜索结果: 'easysep direct'

E. A. Davis et al. (JUN 2018) Physiological reports 6 12 e13745

Evidence for a direct effect of the autonomic nervous system on intestinal epithelial stem cell proliferation.

The sympathetic (SNS) and parasympathetic (PNS) branches of the autonomic nervous system have been implicated in the modulation of the renewal of many tissues,including the intestinal epithelium. However,it is not known whether these mechanisms are direct,requiring an interaction between autonomic neurotransmitters and receptors on proliferating epithelial cells. To evaluate the existence of a molecular framework for a direct effect of the SNS or PNS on intestinal epithelial renewal,we measured gene expression for the main autonomic neurotransmitter receptors in this tissue. We separately evaluated intestinal epithelial regions comprised of the stem,progenitor,and mature cells,which allowed us to investigate the distinct contributions of each cell population to this proposed autonomic effect. Notably,we found that the stem cells expressed the receptors for the SNS-associated alpha2A adrenoreceptor and the PNS-associated muscarinic acetylcholine receptors (M1 and M3). In a separate experiment,we found that the application of norepinephrine or acetylcholine decreases the expression of cyclin D1,a gene necessary for cell cycle progression,in intestinal epithelial organoids compared with controls (P {\textless} 0.05). Together,these results provide evidence of a direct mechanism for the autonomic nervous system influence on intestinal epithelial stem cell proliferation. View Publication

产品类型：

产品号#：

06005

产品名：

IntestiCult™ 类器官生长培养基 (小鼠)

D. R. McHugh et al. ( 2018) PloS one 13 6 e0199573

A G542X cystic fibrosis mouse model for examining nonsense mutation directed therapies.

Nonsense mutations are present in 10{\%} of patients with CF,produce a premature termination codon in CFTR mRNA causing early termination of translation,and lead to lack of CFTR function. There are no currently available animal models which contain a nonsense mutation in the endogenous Cftr locus that can be utilized to test nonsense mutation therapies. In this study,we create a CF mouse model carrying the G542X nonsense mutation in Cftr using CRISPR/Cas9 gene editing. The G542X mouse model has reduced Cftr mRNA levels,demonstrates absence of CFTR function,and displays characteristic manifestations of CF mice such as reduced growth and intestinal obstruction. Importantly,CFTR restoration is observed in G542X intestinal organoids treated with G418,an aminoglycoside with translational readthrough capabilities. The G542X mouse model provides an invaluable resource for the identification of potential therapies of CF nonsense mutations as well as the assessment of in vivo effectiveness of these potential therapies targeting nonsense mutations. View Publication

产品类型：

产品号#：

06005

产品名：

IntestiCult™ 类器官生长培养基 (小鼠)

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

Allan AL et al. (MAY 2005) Cytometry. Part A : the journal of the International Society for Analytical Cytology 65 1 4--14

Detection and quantification of circulating tumor cells in mouse models of human breast cancer using immunomagnetic enrichment and multiparameter flow cytometry.

BACKGROUND: Circulating tumor cells (CTCs) in the peripheral blood of breast cancer patients may be an important indicator of metastatic disease and poor prognosis. However,the use of experimental models is required to fully elucidate the functional consequences of CTCs. The purpose of this study was to optimize the sensitivity of multiparameter flow cytometry for detection of human tumor cells in mouse models of breast cancer. METHODS: MDA-MB-468 human breast cancer cells were serially diluted in whole mouse blood. Samples were lysed and incubated with a fluorescein isothiocyanate-conjugated anti-human leukocytic antigen antibody and a phycoerythrin-conjugated anti-mouse pan-leukocyte CD45 antibody. Samples were then immunomagnetically depleted of CD45-positive leukocytes,fixed,permeabilized,and stained with propidium iodide before flow cytometric analysis. RESULTS: Human breast cancer cells could be differentiated from mouse leukocytes based on increased light scatter,cell surface marker expression,and aneuploid DNA content. The method was found to have a lower sensitivity limit of 10(-5) and was effective for detecting human breast cancer cells in vivo in the circulation of experimental mice carrying primary human mammary tumors. CONCLUSIONS: This technique has the potential to be a valuable and sensitive tool for investigating the biological relevance of CTCs in experimental mouse models of breast cancer. View Publication

产品类型：

产品号#：

18554

18554RF

18564

18564RF

产品名：

技术窍门

组织解离方法指南

Jeselsohn R et al. (JAN 2010) Cancer cell 17 1 65--76

Cyclin D1 kinase activity is required for the self-renewal of mammary stem and progenitor cells that are targets of MMTV-ErbB2 tumorigenesis.

Transplantation studies have demonstrated the existence of mammary progenitor cells with the ability to self-renew and regenerate a functional mammary gland. Although these progenitors are the likely targets for oncogenic transformation,correlating progenitor populations with certain oncogenic stimuli has been difficult. Cyclin D1 is required for lobuloalveolar development during pregnancy and lactation as well as MMTV-ErbB2- but not MMTV-Wnt1-mediated tumorigenesis. Using a kinase-deficient cyclin D1 mouse,we identified two functional mammary progenitor cell populations,one of which is the target of MMTV-ErbB2. Moreover,cyclin D1 activity is required for the self-renewal and differentiation of mammary progenitors because its abrogation leads to a failure to maintain the mammary epithelial regenerative potential and also results in defects in luminal lineage differentiation. View Publication

产品类型：

产品号#：

19757

产品名：

Reutershan J et al. (MAR 2006) The Journal of clinical investigation 116 3 695--702

Critical role of endothelial CXCR2 in LPS-induced neutrophil migration into the lung.

In models of acute lung injury,CXC chemokine receptor 2 (CXCR2) mediates migration of polymorphonuclear leukocytes (PMNs) into the lung. Since CXCR2 ligands,including CXCL1 and CXCL2/3,are chemotactic for PMNs,CXCR2 is thought to recruit PMNs by inducing chemotactic migration. In a model of PMN recruitment to the lung,aerosolized bacterial LPS inhalation induced PMN recruitment to the lung in wild-type mice,but not in littermate CXCR2-/- mice. Surprisingly,lethally irradiated wild-type mice reconstituted with CXCR2-/- BM still showed about 50% PMN recruitment into bronchoalveolar lavage fluid and into lung interstitium,but CXCR2-/- mice reconstituted with CXCR2-/- BM showed no PMN recruitment. Conversely,CXCR2-/- mice reconstituted with wild-type BM showed a surprisingly large defect in PMN recruitment,inconsistent with a role of CXCR2 on PMNs alone. Cell culture,immunohistochemistry,flow cytometry,and real-time RT-PCR were used to show expression of CXCR2 on pulmonary endothelial and bronchial epithelial cells. The LPS-induced increase in lung microvascular permeability as measured by Evans blue extravasation required CXCR2 on nonhematopoietic cells. Our data revealed what we believe to be a previously unrecognized role of endothelial and epithelial CXCR2 in LPS-induced PMN recruitment and lung injury. View Publication

产品类型：

产品号#：

18556

18556RF

产品名：

Xaymardan M et al. (AUG 2009) Stem cells (Dayton,Ohio) 27 8 1911--20

c-Kit function is necessary for in vitro myogenic differentiation of bone marrow hematopoietic cells.

In recent years,the differentiation of bone marrow cells (BMCs) into myocytes has been extensively investigated,but the findings remain inconclusive. The purpose of this study was to determine the conditions necessary to induce myogenic differentiation in short-term cultures of adult BMCs,and to identify the BMC subpopulation responsible for this phenomenon. We report that high-density cultures of murine hematopoietic BMCs gave rise to spontaneous beating cell clusters in the presence of vascular endothelial and fibroblast growth factors. These clusters originated from c-kit(pos) cells. The formation of the clusters could be completely blocked by adding a c-kit/tyrosine kinase inhibitor,Gleevec (imatinib mesylate; Novartis International,Basel,Switzerland,http://www.novartis.com),to the culture. Cluster formation was also blunted in BMCs from c-kit-deficient (Kit(W)/Kit(W-v)) mice. Clustered cells expressed cardiomyocyte-specific transcription factor genes Gata-4 and Nkx2.5,sarcomeric proteins beta-MHC and MLC-2v,and ANF and connexin-43. Immunostaining revealed alpha-sarcomeric actinin expression in more than 90% of clustered cells. Under electron microscopy,the clustered cells exhibited a sarcomeric myofiber arrangement and z-bands. This study defines the microenvironment required to achieve a reproducible in vitro model of beating,myogenic cell clusters. This model could be used to examine the mechanisms responsible for the postnatal myogenic differentiation of BMCs. Our results identify c-kit(pos) bone marrow hematopoietic cells as the source of the myogenic clusters. View Publication

产品类型：

产品号#：

18757

18757RF

产品名：

EasySep™小鼠CD117（cKIT）正选试剂盒

RoboSep™ 小鼠CD117（cKIT）正选试剂盒含滤芯吸头

Pond AC et al. ( 2013) Stem cells (Dayton,Ohio) 31 1 10.1002/stem.1266

Fibroblast Growth Factor Receptor Signaling Is Essential for Normal Mammary Gland Development and Stem Cell Function

Fibroblast growth factor (FGF) signaling plays an important role in embryonic stem cells and adult tissue homeostasis,but the function of FGFs in mammary gland stem cells is less well defined. Both FGFR1 and FGFR2 are expressed in basal and luminal mammary epithelial cells (MECs),suggesting that together they might play a role in mammary gland development and stem cell dynamics. Previous studies have demonstrated that the deletion of FGFR2 resulted only in transient developmental defects in branching morphogenesis. Using a conditional deletion strategy,we investigated the consequences of FGFR1 deletion alone and then the simultaneous deletion of both FGFR1 and FGFR2 in the mammary epithelium. FGFR1 deletion using a keratin 14 promoter-driven Cre-recombinase resulted in an early,yet transient delay in development. However,no reduction in functional outgrowth potential was observed following limiting dilution transplantation analysis. In contrast,a significant reduction in outgrowth potential was observed upon the deletion of both FGFR1 and FGFR2 in MECs using adenovirus-Cre. Additionally,using a fluorescent reporter mouse model to monitor Cre-mediated recombination,we observed a competitive disadvantage following transplantation of both FGFR1/R2-null MECs,most prominently in the basal epithelial cells. This correlated with the complete loss of the mammary stem cell repopulating population in the FGFR1/R2-attenuated epithelium. FGFR1/R2-null MECs were partially rescued in chimeric outgrowths containing wild-type MECs,suggesting the potential importance of paracrine mechanisms involved in the maintenance of the basal epithelial stem cells. These studies document the requirement for functional FGFR signaling in mammary stem cells during development. View Publication

产品类型：

产品号#：

19758

60099

60099.1

60099AD

60099AD.1

60099AZ

60099AZ.1

60099BT

60099BT.1

60099FI

60099FI.1

60099PE

60099PE.1

60099PS

60099PS.1

60037

60037AD

60037AD.1

60037AZ

60037AZ.1

60037BT

60037BT.1

60037FI

60037FI.1

60037PE

60037PE.1

60037PB

60037PB.1

产品名：

抗小鼠CD24抗体，clone M1/69

抗小鼠CD24抗体，clone M1/69，Alexa Fluor® 488

抗小鼠CD24抗体，clone M1/69，APC

抗小鼠CD24抗体，clone M1/69，Biotin

抗小鼠CD24抗体，clone M1/69，PE

抗小鼠CD24抗体，clone M1/69，PerCP-Cy5.5

抗小鼠CD49f抗体，clone GoH3

抗小鼠CD49f抗体，clone GoH3，Alexa Fluor® 488

抗小鼠CD49f抗体，clone GoH3，APC

抗小鼠CD49f抗体，clone GoH3，Biotin

抗小鼠CD49f抗体，clone GoH3，FITC

抗小鼠CD49f抗体，clone GoH3，PE

抗小鼠CD49f抗体，clone GoH3，Pacific Blue™

Luo M et al. (JAN 2009) Cancer research 69 2 466--74

Mammary epithelial-specific ablation of the focal adhesion kinase suppresses mammary tumorigenesis by affecting mammary cancer stem/progenitor cells.

Focal adhesion kinase (FAK) has been implicated in the development of cancers,including those of the breast. Nevertheless,the molecular and cellular mechanisms by which FAK promotes mammary tumorigenesis in vivo are not well understood. Here,we show that targeted deletion of FAK in mouse mammary epithelium significantly suppresses mammary tumorigenesis in a well-characterized breast cancer model. Ablation of FAK leads to the depletion of a subset of bipotent cells in the tumor that express both luminal marker keratin 8/18 and basal marker keratin 5. Using mammary stem/progenitor markers,including aldehyde dehydrogenase,CD24,CD29,and CD61,we further revealed that ablation of FAK reduced the pool of cancer stem/progenitor cells in primary tumors of FAK-targeted mice and impaired their self-renewal and migration in vitro. Finally,through transplantation in NOD-SCID mice,we found that cancer stem/progenitor cells isolated from FAK-targeted mice have compromised tumorigenicity and impaired maintenance in vivo. Together,these results show a novel function of FAK in maintaining the mammary cancer stem/progenitor cell population and provide a novel mechanism by which FAK may promote breast cancer development and progression. View Publication

产品类型：

产品号#：

18556

18556RF

产品名：

Stingl J et al. (MAR 2006) Nature 439 7079 993--7

Purification and unique properties of mammary epithelial stem cells.

Elucidation of the cellular and molecular mechanisms that maintain mammary epithelial tissue integrity is of broad interest and paramount to the design of more effective treatments for breast cancer. Evidence from both in vitro and in vivo experiments suggests that mammary cell differentiation is a hierarchical process originating in an uncommitted stem cell with self-renewal potential. However,analysis of the properties and regulation of mammary stem cells has been limited by a lack of methods for their prospective isolation. Here we report the use of multi-parameter cell sorting and limiting dilution transplant analysis to demonstrate the purification of a rare subset of adult mouse mammary cells that are able individually to regenerate an entire mammary gland within 6 weeks in vivo while simultaneously executing up to ten symmetrical self-renewal divisions. These mammary stem cells are phenotypically distinct from and give rise to mammary epithelial progenitor cells that produce adherent colonies in vitro. The mammary stem cells are also a rapidly cycling population in the normal adult and have molecular features indicative of a basal position in the mammary epithelium. View Publication

产品类型：

产品号#：

19757

产品名：

搜索结果: 'easysep direct'

Evidence for a direct effect of the autonomic nervous system on intestinal epithelial stem cell proliferation.

A G542X cystic fibrosis mouse model for examining nonsense mutation directed therapies.

Detection and quantification of circulating tumor cells in mouse models of human breast cancer using immunomagnetic enrichment and multiparameter flow cytometry.

Cyclin D1 kinase activity is required for the self-renewal of mammary stem and progenitor cells that are targets of MMTV-ErbB2 tumorigenesis.

Critical role of endothelial CXCR2 in LPS-induced neutrophil migration into the lung.

c-Kit function is necessary for in vitro myogenic differentiation of bone marrow hematopoietic cells.

Fibroblast Growth Factor Receptor Signaling Is Essential for Normal Mammary Gland Development and Stem Cell Function

Mammary epithelial-specific ablation of the focal adhesion kinase suppresses mammary tumorigenesis by affecting mammary cancer stem/progenitor cells.

Purification and unique properties of mammary epithelial stem cells.

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