Millipore Sigma Vibrant Logo
 

cell-


15505 Results Advanced Search  
Showing
Products (4,713)
Documents (9,921)
Site Content (871)

Narrow Your Results Use the filters below to refine your search

Document Type

  • (9,159)
  • (408)
  • (111)
  • (110)
  • (34)
  • Show More
Can't Find What You're Looking For?
Contact Customer Service

 

  • Large cell anaplastic medulloblastoma metastatic to the scalp: tumor and derived stem-like cells features. 24739212

    Extraneural metastases (ENM) rarely occur in medulloblastoma (MBL) patients and only few cases of subcutaneous localizations have been described. ENM indicate an aggressive disease associated with a worse prognosis. The characterization of metastatic tumours might be useful to understand their pathogenesis and to identify the most appropriate therapeutic strategies.We present the case of a child with Large Cell Anaplastic (LC/A) MBL, who developed multiple subcutaneous metastases in the scalp area after a ventriculo-peritoneal shunting procedure. The disease rapidly progressed and the child died despite chemotherapy and primary tumour surgical debulking.We molecularly classified the tumour as a group 3 MBL; in addition, we derived stem-like cells (SLC) from a metastatic lesion. Primary tumour, metastases and SLC were further analysed, particularly focusing on features linked to the cutaneous dissemination. Indeed, molecules involved in angiogenesis, cell invasion and epidermal growth factor signalling resulted highly expressed.The present report describes a very rare case of subcutaneous metastatic MBL. The tumour, metastases and SLC have been clinically, pathologically and molecularly characterized. Our case is an example of multidisciplinary approach aiming to characterize MBL aggressive behaviour.
    Document Type:
    Reference
    Product Catalog Number:
    MAB4343
    Product Catalog Name:
    Anti-SOX-2 Antibody

  • The Cell Adhesion Molecule Necl-4/CADM4 Serves as a Novel Regulator for Contact Inhibition of Cell Movement and Proliferation. 25893857

    Contact inhibition of cell movement and proliferation is critical for proper organogenesis and tissue remodeling. We show here a novel regulatory mechanism for this contact inhibition using cultured vascular endothelial cells. When the cells were confluently cultured, Necl-4 was up-regulated and localized at cell-cell contact sites where it cis-interacted with the vascular endothelial growth factor (VEGF) receptor. This interaction inhibited the tyrosine-phosphorylation of the VEGF receptor through protein-tyrosine phosphatase, non-receptor type 13 (PTPN13), eventually reducing cell movement and proliferation. When the cells were sparsely cultured, Necl-4 was down-regulated but accumulated at leading edges where it inhibited the activation of Rho-associated protein kinase through PTPN13, eventually facilitating the VEGF-induced activation of Rac1 and enhancing cell movement. Necl-4 further facilitated the activation of extracellular signal-regulated kinase 1/2, eventually enhancing cell proliferation. Thus, Necl-4 serves as a novel regulator for contact inhibition of cell movement and proliferation cooperatively with the VEGF receptor and PTPN13.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1501
    Product Catalog Name:
    Anti-Actin Antibody, clone C4

  • T cell metabolism. The protein LEM promotes CD8⁺ T cell immunity through effects on mitochondrial respiration. 25883318

    Protective CD8(+) T cell-mediated immunity requires a massive expansion in cell number and the development of long-lived memory cells. Using forward genetics in mice, we identified an orphan protein named lymphocyte expansion molecule (LEM) that promoted antigen-dependent CD8(+) T cell proliferation, effector function, and memory cell generation in response to infection with lymphocytic choriomeningitis virus. Generation of LEM-deficient mice confirmed these results. Through interaction with CR6 interacting factor (CRIF1), LEM controlled the levels of oxidative phosphorylation (OXPHOS) complexes and respiration, resulting in the production of pro-proliferative mitochondrial reactive oxygen species (mROS). LEM provides a link between immune activation and the expansion of protective CD8(+) T cells driven by OXPHOS and represents a pathway for the restoration of long-term protective immunity based on metabolically modified cytotoxic CD8(+) T cells.
    Document Type:
    Reference
    Product Catalog Number:
    17-371
    Product Catalog Name:
    EZ-ChIP™

  • T cell activation regulates CD6 alternative splicing by transcription dynamics and SRSF1. 24890719

    The T cell-surface glycoprotein CD6 is a modulator of cellular responses and has been implicated in several autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and psoriasis. During Ag presentation, CD6 is targeted to the immunological synapse in a ligand binding-dependent manner, in which CD6 domain 3 directly contacts CD166, expressed on the APC. T cell activation results in the induction of CD6Δd3, an alternatively spliced isoform that lacks the ligand-binding domain and thus no longer localizes at the immunological synapse. In this study, we investigated the molecular mechanisms regulating the expression of CD6Δd3 upon human primary T cell activation. Using chromatin immunoprecipitation, we observed an increase in RNA polymerase II occupancy along the CD6 gene and augmented CD6 transcription. We showed that activation leads to transcription-related chromatin modifications, revealed by higher CD6 acetylation levels. Modulation of chromatin conformation using a histone deacetylase inhibitor that increases transcription rate causes an increase of exon 5 skipping. We further showed that the splicing factor SRSF1 binds to a regulatory element in CD6 intron 4, activating exon 5 splicing and promoting exon 5 inclusion. Concomitant with T cell activation-induced exon 5 skipping, we observed a downregulation of SRSF1. Using RNA immunoprecipitation, we showed that in activated T cells, SRSF1 recruitment to the CD6 transcript is impaired by increased chromatin acetylation levels. We propose that upon T cell activation, SRSF1 becomes limiting, and its function in CD6 exon 5 splicing is countered by an increase in CD6 transcription, dependent on chromatin acetylation.
    Document Type:
    Reference
    Product Catalog Number:
    17-701
    Product Catalog Name:
    EZ-Magna RIP™ RNA-Binding Protein Immunoprecipitation Kit

  • Mast cell activation and degranulation promotes renal fibrosis in experimental unilateral ureteric obstruction. 22673890

    Progressive renal fibrosis is the final common pathway leading to renal failure irrespective of the initiating cause. Clinical studies of renal fibrosis found that prominent mast cell accumulation correlated with worse outcomes. Mast cells are pluripotent innate immune cells that synthesize and secrete profibrotic mediators. Here we use mast cell-deficient (Kit(W-sh/W-sh)) mice to define a functional pathogenic role for these cells in the development of renal fibrosis. Intrarenal collagen deposition was significantly decreased in mast cell-deficient compared to wild-type mice 7 and 14 days after unilateral ureteric obstruction. The intrarenal expression of mRNAs for transforming growth factor-β, α-smooth muscle actin, chemokines, and renal macrophages and CD4(+) T cells were also decreased in mast cell-deficient mice. Reconstitution of the mast cell population in mast cell-deficient mice with wild-type bone marrow-derived mast cells restored the pattern and intensity of renal fibrosis to levels seen in wild-type mice following ureteric ligation. Interestingly, the mast cells were recruited, activated, and degranulated within 6 h of ureteric ligation. A mast cell stabilizer that impairs degranulation, disodium chromoglycate, significantly attenuated renal fibrosis following ureteric ligation in wild-type mice. Thus, mast cells promote renal fibrosis and their targeting may offer therapeutic potential in the treatment of renal fibrosis.
    Document Type:
    Reference
    Product Catalog Number:
    IMM001

  • Glial cell line-derived neurotrophic factor-secreting human neural progenitors show long-term survival, maturation into astrocytes, and no tumor formation following trans ... 24284956

    Human neural progenitor cells (hNPCs) derived from the fetal cortex can be expanded in vitro and genetically modified through lentiviral transduction to secrete growth factors shown to have a neurotrophic effect in animal models of neurological disease. hNPCs survive and mature following transplantation into the central nervous system of large and small animals including the rat model of amyotrophic lateral sclerosis. Here we report that hNPCs engineered to express glial cell line-derived neurotrophic factor (GDNF) survive long-term (7.5 months) following transplantation into the spinal cord of athymic nude rats and continue to secrete GDNF. Cell proliferation declined while the number of astrocytes increased, suggesting final maturation of the cells over time in vivo. Together these data show that GDNF-producing hNPCs may be useful as a source of cells for long-term delivery of both astrocytes and GDNF to the damaged central nervous system.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Mast cell subpopulations in the synovial tissue of patients with osteoarthritis: selective increase in numbers of tryptase-positive, chymase-negative mast cells. 9875142

    Although there is relatively little evidence of inflammation in osteoarthritis (OA), increases in mast cell numbers and mast cell activation are prominent features of the synovial tissue. As little is known of the types of mast cells which may be involved, the numbers and distribution of mast cell subpopulations have been investigated as defined according to their content of proteases. Tissue was obtained from patients with OA undergoing total knee replacement surgery (n = 14) and from control subjects either post-mortem (n = 11) or following leg amputation for peripheral vascular disease (n = 3); a double-labelling immunocytochemical procedure with monoclonal antibodies specific for tryptase and chymase was applied to identify those mast cells which contain both tryptase and chymase (MCTC) and those with tryptase but not chymase (MCT). There was considerable variation between individual tissues and between sites of tissue sampling, but cells of the MCTC subset were predominant in the synovial layer of both groups of subjects without joint disease, accounting for some 60 per cent of all mast cells present. In tissue from OA patients, however, there appeared to have been a striking shift in the relative proportions of mast cells from the MCTC to the MCT phenotype, with many more MCT cells present in the synovial tissues of OA patients (median 53 MCT/mm2) than in tissue from post-mortem (7.5 MCT/mm2, P < 0.0001) or amputation controls (12 MCT/mm2). In contrast, numbers of synovial MCTC cells in the synovium of OA patients (20 MCTC/mm2) differed little from those in either of the control groups (both 12 MCTC/mm2). In several other conditions, the MCT cells have been linked with inflammatory events, but it seems that in OA, other factors may be operating to induce a selective expansion of this subpopulation.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Glial cell line-derived neurotrophic factor-mediated enteric neuronal survival involves glycogen synthase kinase-3beta phosphorylation and coupling with 14-3-3. 16996218

    Glial cell line-derived neurotrophic factor (GDNF) promotes the growth and survival of enteric neurons, but the mechanisms involved are poorly understood. GDNF is known to promote the survival of enteric neurons through activation of the PI3-Kinase/Akt signaling pathway. We investigated the role of glycogen synthase kinase-3beta (GSK-3beta) in enteric neuronal survival, and the ability of GDNF to regulate the activity of GSK-3beta using primary rat embryonic enteric neurons. GDNF, through activation of the PI3-kinase pathway enhanced the phosphorylation of GSK-3beta at its N-terminal serine-9 residue, and promoted the association of GSK-3beta with 14-3-3. Transfection of a constitutively active S9A-GSK-3beta mutant prevented the survival effects of GDNF, whereas a dominant negative GSK-3beta construct prevented GDNF withdrawal-induced cell death. Increased GSK-3beta activity was associated with an increase in tau phosphorylation. Thus, GDNF promotes enteric neuronal survival by modulating GSK-3beta and its downstream target tau. Inhibitors of GSK-3beta activity may have therapeutic potential in improving enteric neuronal survival.
    Document Type:
    Reference
    Product Catalog Number:
    MAB365
    Product Catalog Name:
    Anti-Nerve Growth Factor Receptor Antibody, extracellular, clone 192-IgG