다음 MAP메이트™는 통합될 수 없습니다: -다른 분석 완충용액이 필요한 MAP메이트™. -인산 특이성 및 총 MAP메이트™ 조합, 예: 총 GSK3β 및 GSK3β(Ser 9). -PanTyr 및 자리 특이성 MAP메이트™, 예: Phospho-EGF 수용체 및 phospho-STAT1(Tyr701). -단일 표적(Akt, STAT3)를 위한 1개 이상의 1 phospho-MAP메이트™. - GAPDH 및 β-Tubulin은 panTyr를 포함하는 키트 또는 MAP메이트™와 통합될 수 없습니다.
Custom Premix Selecting "Custom Premix" option means that all of the beads you have chosen will be premixed in manufacturing before the kit is sent to you.
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96-Well Plate
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다른 시약 추가 (MAP메이트 사용을 위해 완충용액과 검출 키트가 필요함)
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
공간 절약 옵션 다수의 키트를 구매하시는 고객은 고용량 저장을 위해 키트 포장을 제거하고 비닐백에 담긴 멀티플레스 분석 구성품을 받아 저장 공간을 절약하도록 선택할 수 있습니다.
이 제품은 즐겨찾기에 저장되었습니다.
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이제 다른 키트를 사용자 지정하거나, 사전 혼합된 키트를 선택하거나, 결재하거나 또는 주문 도구를 종료할 수 있습니다.
Disruption of cerebellar granular neuronal precursor (GNP) maturation can result in defects in motor coordination and learning, or in medulloblastoma, the most common childhood brain tumor. The Sonic Hedgehog (Shh) pathway is important for GNP proliferation; however, the factors regulating the extent and timing of GNP proliferation, as well as GNP differentiation and migration are poorly understood. The p53 tumor suppressor has been shown to negatively regulate the activity of the Shh effector, Gli1, in neural stem cells; however, the contribution of p53 to the regulation of Shh signaling in GNPs during cerebellar development has not been determined. Here, we exploited a hypomorphic allele of Mdm2 (Mdm2(puro)), which encodes a critical negative regulator of p53, to alter the level of wild-type MDM2 and p53 in vivo. We report that mice with reduced levels of MDM2 and increased levels of p53 have small cerebella with shortened folia, reminiscent of deficient Shh signaling. Indeed, Shh signaling in Mdm2-deficient GNPs is attenuated, concomitant with decreased expression of the Shh transducers, Gli1 and Gli2. We also find that Shh stimulation of GNPs promotes MDM2 accumulation and enhances phosphorylation at serine 166, a modification known to increase MDM2-p53 binding. Significantly, loss of MDM2 in Ptch1(+/-) mice, a model for Shh-mediated human medulloblastoma, impedes cerebellar tumorigenesis. Together, these results place MDM2 at a major nexus between the p53 and Shh signaling pathways in GNPs, with key roles in cerebellar development, GNP survival, cerebellar foliation, and MB tumorigenesis.
문서 타입:
Reference
카탈로그 번호:
S7100
제품명:
ApopTag® Peroxidase In Situ Apoptosis Detection Kit
Huangqi decoction was first described in Prescriptions of the Bureau of Taiping People's Welfare Pharmacy in Song Dynasty (AD 1078), and it is an effective recipe that is usually used to treat consumptive disease, anorexia, and chronic liver diseases. Transforming growth factor beta 1 (TGFβ1) plays a key role in the progression of liver fibrosis, and Huangqi decoction and its ingredients (IHQD) markedly ameliorated hepatic fibrotic lesions induced by ligation of the common bile duct (BDL). However, the mechanism of IHQD on hepatic fibrotic lesions is not yet clear. The purpose of the present study is to elucidate the roles of TGFβ1 activation, Smad-signaling pathway, and extracellular signal-regulated kinase (ERK) in the pathogenesis of biliary fibrosis progression and the antifibrotic mechanism of IHQD.
Serotonin receptors (5-HT4Rs) are critical to both short-term and long-term memory processes. These receptors mainly trigger the cyclic adenosine monophosphate (cAMP)/protein kinase A signaling pathway, which is regulated by cAMP phosphodiesterases (PDEs).
문서 타입:
Reference
카탈로그 번호:
03-114
제품명:
RIPAb+ Musashi 1 - RIP Validated Antibody and Primer Set, rabbit monoclonal
OBJECTIVE: Cord blood banks provide fully human leukocyte antigen-typed cells, from which a set of standard induced pluripotent stem (iPS) cells for use in allogenic transplantation can be derived. Hence, the ability to generate iPS cells from cord blood cells has the potential to provide a suitable source for clinical transplantation. The aim of this work is to determine the reprogramming methods, culture conditions, and cell fractions that can be used to generate iPS cells from cord blood cells effectively. MATERIALS AND METHODS: CD34(+), mononucleated, and derived adherent cells from cord blood were cultured in hematopoietic medium (X-vivo10 containing 50 ng/mL interleukin-6, 50 ng/mL soluble interleukin-6 receptor, 50 ng/mL stem cell factor, 10 ng/mL thrombopoietin, and 20 ng/mL Flit3/4 ligand) 3 days prior to viral infection. Cells were then infected with retroviral constructs driving the expression of OCT3/4, SOX2, Krüppel-like factor 4, c-MYC, and enhanced green fluorescent protein together with or without the p53 knockdown lentiviral construct Shp53 pLKO.1-puro. Infected cells were then cultured for an additional 4 days in hematopoietic culture medium before being transferred onto mouse embryonic fibroblast (MEF) or SNL76/7 feeder cells in human embryonic stem cell medium (Dulbecco's modified Eagle medium/F-12 containing 20% knockout serum replacement, 200 mM L-glutamine, 1% non-essential amino acids (NEAA), 0.1 mM 2-mercaptoethanol, and 4 ng/mL basic fibroblast growth factor). Subsequently, the number of embryonic stem cell-like colonies that emerged in the following 4 weeks was scored. Expression of a number of pluripotency makers were examined by immunochemistry and reverse transcriptase polymerase chain reaction. Finally, the differentiation potential of selected colonies was determined by teratoma formation in severe combined immunodeficient mice and in vitro culture. RESULTS: Repression of p53 expression by the addition of a lentiviral p53 short-hairpin RNA expression vector increased the frequency of formation of iPS-like colonies from 1 (on average) to around 100 per 2 x 10(4) cells when infected cells were grown on SNL feeder cells. CONCLUSIONS: iPS cells can be generated easily from CD34(+) cord blood cells through the addition of p53 inhibition to standard reprogramming conditions.