Millipore Sigma Vibrant Logo
 

35899-43-5


71 Results Gelişmiş Arama  
Showing
Products (0)
Dokümanlar (71)
Site Content (0)

Sonuçlarınızı Daraltın Use the filters below to refine your search

Aradığınızı Bulamadınız mı?
Müşteri Hizmetleri ile
İletişime Geçin

 
MilliporeSigma Documents

Doküman ararken yardıma ihtiyacınız var mı?

  • Analiz sertifikaları, Kalite Sertifikaları veya Güvenlik Bilgi Formlarını aramak için Doküman Arayıcı’yı kullanmayı deneyin.
     
  • Kullanım Kılavuzlarına erişmek için yardıma ihtiyacınız olur ise Müşteri Hizmetleri ile iletişime geçebilirsiniz.
  • Certificate of Analysis 516724_3589945

    Document Type:
    Certificate of Analysis
    Lot Number:
    3589945
    Product Catalog Number:
    516724
    Product Catalog Name:
    Phenol, Molecular Biology Grade - CAS 108-95-2 - Calbiochem
  • Certificate of Analysis 361507_3589935

    Document Type:
    Certificate of Analysis
    Lot Number:
    3589935
    Product Catalog Number:
    361507
    Product Catalog Name:
    Glycogen, Molecular Biology Grade, Mussel - CAS 9005-79-2 - Calbiochem
  • DNA damage response is suppressed by the high cyclin-dependent kinase 1 activity in mitotic mammalian cells. 21878640

    DNA damage response (DDR) is vital for genomic stability, and its deficiency is linked to tumorigenesis. Extensive studies in interphase (G(1)-S-G(2)) mammalian cells have revealed the mechanisms of DDR in great detail; however, how mitotic cells respond to DNA damage remains less defined. We report here that a full DDR is suppressed in mitotic mammalian cells until telophase/cytokinesis. Although early DDR markers such as the phosphorylations of ataxia telangiectasia mutated (ATM) and histone H2A.x (H2AX) can be readily detected, the ionizing radiation-induced foci (IRIF) formation of late DDR markers such as breast cancer type 1 susceptibility protein (BRCA1) and p53-binding protein 1 (53BP1) are absent until the telophase/cytokinesis stage. We further showed that the IR-induced ubiquitination cascade around DNA damage sites did not occur in mitotic cells, which explains, at least in part, why BRCA1 and 53BP1 cannot be recruited to the damaged sites. These observations indicate that DDR is suppressed in mitotic cells after the step of γH2AX formation. Not surprisingly, we found that the absence of a full DDR in mitotic cells was associated with the high cyclin-dependent kinase 1 (CDK1) activities. More 53BP1 IRIF could be detected when the irradiated mitotic cells were treated with a CDK1 inhibitor. Further, the activation of CDK5 in interphase cells impedes the formation of 53BP1 IRIF. Together, these results suggest that the DDR is suppressed by the high CDK1 activity in mitotic mammalian cells.
    Document Type:
    Reference
    Product Catalog Number:
    05-636
    Product Catalog Name:
    Anti-phospho-Histone H2A.X (Ser139) Antibody, clone JBW301
  • Regulation of MAPK-activated protein kinase 5 activity and subcellular localization by the atypical MAPK ERK4/MAPK4. 16971392

    MAPK-activated protein kinase 5 (MK5) was recently identified as a physiological substrate of the atypical MAPK ERK3. Complex formation between ERK3 and MK5 results in phosphorylation and activation of MK5, concomitant stabilization of ERK3, and the nuclear exclusion of both proteins. However, ablation of ERK3 in HeLa cells using small interfering RNA or in fibroblasts derived from ERK3 null mice reduces the activity of endogenous MK5 by only 50%, suggesting additional mechanisms of MK5 regulation. Here we identify the ERK3-related kinase ERK4 as a bona fide interaction partner of MK5. Binding of ERK4 to MK5 is accompanied by phosphorylation and activation of MK5. Furthermore, complex formation also results in the relocalization of MK5 from nucleus to cytoplasm. However unlike ERK3, ERK4 is a stable protein, and its half-life is not modified by the presence or absence of MK5. Finally, although knock-down of ERK4 protein in HeLa cells reduces endogenous MK5 activity by approximately 50%, a combination of small interfering RNAs targeting both ERK4 and ERK3 causes a further reduction in the MK5 activity by more than 80%. We conclude that MK5 activation is dependent on both ERK3 and ERK4 in these cells and that these atypical MAPKs are both physiological regulators of MK5 activity.
    Document Type:
    Reference
    Product Catalog Number:
    12-342
    Product Catalog Name:
    Rabbit Anti-Sheep IgG Antibody, HRP conjugate
  • Anti-E6AP - 3899543

    Document Type:
    Certificate of Analysis
    Lot Number:
    3899543
    Product Catalog Number:
    ABS989
    Product Catalog Name:
    Anti-E6AP Antibody
  • Cardiac remodeling and myocardial dysfunction in obese spontaneously hypertensive rats. 22963383

    The additive effects of obesity and metabolic syndrome on left ventricular (LV) maladaptive remodeling and function in hypertension are not characterized.We compared an obese spontaneously hypertensive rat model (SHR-ob) with lean spontaneously hypertensive rats (SHR-lean) and normotensive controls (Ctr). LV-function was investigated by cardiac magnetic resonance imaging and invasive LV-pressure measurements. LV-interstitial fibrosis was quantified and protein levels of phospholamban (PLB), Serca2a and glucose transporters (GLUT1 and GLUT4) were determined by immunohistochemistry.Systolic blood pressure was similar in SHR-lean and SHR-ob (252 ± 7 vs. 242 ± 7 mmHg, p = 0.398) but was higher when compared to Ctr (155 ± 2 mmHg, p less than  0.01 for both). Compared to SHR-lean and Ctr, SHR-ob showed impaired glucose tolerance and increased body-weight. In SHR-ob, LV-ejection fraction was impaired vs. Ctr (46.2 ± 1.1 vs. 59.6 ± 1.9%, p = 0.007). LV-enddiastolic pressure was more increased in SHR-ob than in SHR-lean (21.5 ± 4.1 vs. 5.9 ± 0.81 mmHg, p = 0.0002) when compared to Ctr (4.3 ± 1.1 mmHg, p less than  0.0001 for both), respectively. Increased LV-fibrosis together with increased myocyte diameters and ANF gene expression in SHR-ob were associated with increased GLUT1-protein levels in SHR-ob suggestive for an upregulation of the GLUT1/ANF-axis. Serca2a-protein levels were decreased in SHR-lean but not altered in SHR-ob compared to Ctr. PLB-phosphorylation was not altered.In addition to hypertension alone, metabolic syndrome and obesity adds to the myocardial phenotype by aggravating diastolic dysfunction and a progression towards systolic dysfunction. SHR-ob may be a useful model to develop new interventional and pharmacological treatment strategies for hypertensive heart disease and metabolic disorders.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple
  • Anti-Myostatin, Near CT - 3899545

    Document Type:
    Certificate of Analysis
    Lot Number:
    3899545
    Product Catalog Number:
    AB3239-I
    Product Catalog Name:
    Anti-Myostatin Antibody, Near CT