References
Items 745 to 756 of 7990 total
- Kawada M et al. ( 2006) Cancer research 66 6 2913--2917
Signal transducers and activators of transcription 3 activation is involved in nuclear accumulation of beta-catenin in colorectal cancer.
Nuclear accumulation of beta-catenin is a key event for the development of colorectal cancer. Little is known, however, about the mechanisms underlying translocation of beta-catenin from the cytoplasm or the membrane to the nucleus. The present study examined whether signal transducers and activators of transcription 3 (STAT3) activation is involved in the nuclear accumulation of beta-catenin in colorectal cancer cells. Of the 90 primary colorectal cancer tissues, 40 (44.4%) were positive for nuclear staining of p-STAT3 and 63 (70.0%) were positive for nuclear staining of beta-catenin. The nuclear staining of both p-STAT3 and beta-catenin were observed predominantly in the periphery of the cancer tissues. Importantly, of the 40 tumors with p-STAT3 nuclear staining, 37 (92.5%) were also positive for nuclear beta-catenin staining and there was a significant correlation between p-STAT3 and beta-catenin nuclear staining (P textless 0.01). Coexpression of nuclear p-STAT3 and beta-catenin was associated with lower patient survival (P textless 0.01). In an in vitro study using a human colon cancer cell line, SW480, inhibition of STAT3 by dominant negative STAT3 or the Janus kinase inhibitor, AG490, induced translocation of beta-catenin from the nucleus to the cytoplasm or membrane. Luciferase assays revealed that STAT3 inhibition resulted in significant suppression of beta-catenin/T-cell factor transcription in association with significant inhibition of cell proliferation (P textless 0.05). These findings suggest that in colorectal cancer, STAT3 activation is involved in the nuclear accumulation of beta-catenin, resulting in poor patient survival.Catalog #: Product Name: 72932 AG-490 Catalog #: 72932 Product Name: AG-490 Wu W et al. (JUL 2006) Blood 108 1 141--51KSHV/HHV-8 infection of human hematopoietic progenitor (CD34+) cells: persistence of infection during hematopoiesis in vitro and in vivo.
The cellular reservoir for Kaposi sarcoma-associated herpesvirus (KSHV) infection in the hematopoietic compartment and mechanisms governing latent infection and reactivation remain undefined. To determine susceptibility of human CD34+ hematopoietic progenitor cells (HPCs) to infection with KSHV, purified HPCs were exposed to KSHV, and cells were differentiated in vitro and in vivo. Clonogenic colony-forming activity was significantly suppressed in KSHV-infected CD34+ cells, and viral DNA was predominantly localized to granulocyte-macrophage colonies differentiated in vitro. rKSHV.219 is a recombinant KSHV construct that expresses green fluorescent protein from a cellular promoter active during latency and red fluorescent protein from a viral lytic promoter. Infection of CD34+ HPCs with rKSHV.219 showed similar patterns of infection, persistence, and hematopoietic suppression in vitro in comparison with KSHV. rKSHV.219 infection was detected in human CD14+ and CD19+ cells recovered from NOD/SCID mouse bone marrow and spleen following reconstitution with rKSHV.219-infected CD34+ HPCs. These results suggest that rKSHV.219 establishes persistent infection in NOD/SCID mice and that virus may be disseminated following differentiation of infected HPCs into the B-cell and monocyte lineages. CD34+ HPCs may be a reservoir for KSHV infection and may provide a continuous source of virally infected cells in vivo.Catalog #: Product Name: 02690 StemSpanâ„¢ CC100 Catalog #: 02690 Product Name: StemSpanâ„¢ CC100 Koul D et al. ( 2006) Molecular cancer therapeutics 5 3 637--644Inhibition of Akt survival pathway by a small-molecule inhibitor in human glioblastoma.
Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and Akt are important regulators of the phosphatidylinositol 3-kinase (PI3K) pathway and thus are important to the regulation of a wide spectrum of tumor-related biological processes. Akt regulates several critical cellular functions, including cell cycle progression; cell migration, invasion, and survival; and angiogenesis. Decreased expression of PTEN and overexpression of the Akt proto-oncogene, which is located downstream of PI3K, have been shown in a variety of cancers, including glioblastoma. Novel small-molecule inhibitors of receptors and signaling pathways, including inhibitors of the PI3K pathway, have shown antitumor activity, but inhibitors of Akt have not been examined. In this study, we tested our hypothesis that the pharmacologic inhibition of Akt has an antiproliferative effect on gliomas. We showed that two newly developed Akt inhibitors, KP-372-1 and KP-372-2 (herein called KP-1 and KP-2), effectively inhibited the PI3K/Akt signaling cascade. KP-1 and KP-2 blocked both the basal and epidermal growth factor-induced phosphorylation of Akt Ser473 at 125 and 250 nmol/L, which, in turn, reduced the activation of intracellular downstream targets of Akt, including GSK-3beta and p70s6k. Furthermore, the treatment of U87 and U251 glioma cells with 125 to 250 nmol/L KP-1 and KP2 for 48 hours inhibited cell growth by approximately 50%. This decrease in cell growth stemmed from the induction of apoptosis. Collectively, these results provide a strong rationale for the pharmacologic targeting of Akt for the treatment of gliomas.Staton PJ et al. (APR 2006) Journal of immunology (Baltimore, Md. : 1950) 176 7 3978--86IL-7 is a critical factor in modulating lesion development in Skn-directed autoimmunity.
In a murine model of autoimmunity targeted against the epidermal cell Ags, Skn, adoptive transfer of Skn-immune T cells to immunosuppressed recipients elicits skin lesions in areas of mild epidermal trauma. In this study, we examined peripheral regulation of Skn-induced autoreactivity disrupted by rendering the mice immunoincompetent. We found that regulation of Skn-directed autoimmunity was restored by cotransfer of normal syngeneic spleen cells at twice the concentration of Skn-immune cells and was evidenced by significantly reduced lesion severity by days 5-7 post-cotransfer compared with animals given injections of Skn-immune cells alone. Enrichment and depletion of normal CD4(+) or CD8(+) spleen cells and RT-PCR analysis of selected cytokines identified CD4(+) cells as the regulatory cells in the cotransfer inoculum; however, significant reduction in lesion severity was observed only when there was a concomitant increase in levels of IL-7. The role of IL-7 was further supported in that mice cotransferred with Skn-immune cells plus normal spleen cells, but also treated with anti-IL-7 Ab, no longer exhibited reduced lesion severity. To determine whether IL-7 expression without normal spleen cell cotransfer could modulate lesion development, an IL-7-encoding plasmid (pCMV-Tag1-IL-7) was topically delivered to sites flanking the stressed skin site in Skn-induced autoimmune mice. Daily application of 15 mug of pCMV-Tag1-IL-7 significantly suppressed lesion severity. Our results support a mechanism for CD4(+) T cells and IL-7 in contributing to the control of autoreactivity.Chen W et al. (JUL 2006) Blood 108 2 669--77A murine Mll-AF4 knock-in model results in lymphoid and myeloid deregulation and hematologic malignancy.
The 2 most frequent human MLL hematopoietic malignancies involve either AF4 or AF9 as fusion partners; each has distinct biology but the role of the fusion partner is not clear. We produced Mll-AF4 knock-in (KI) mice by homologous recombination in embryonic stem cells and compared them with Mll-AF9 KI mice. Young Mll-AF4 mice had lymphoid and myeloid deregulation manifest by increased lymphoid and myeloid cells in hematopoietic organs. In vitro, bone marrow cells from young mice formed unique mixed pro-B lymphoid (B220(+)CD19(+)CD43(+)sIgM(-), PAX5(+), TdT(+), IgH rearranged)/myeloid (CD11b/Mac1(+), c-fms(+), lysozyme(+)) colonies when grown in IL-7- and Flt3 ligand-containing media. Mixed lymphoid/myeloid hyperplasia and hematologic malignancies (most frequently B-cell lymphomas) developed in Mll-AF4 mice after prolonged latency; long latency to malignancy indicates that Mll-AF4-induced lymphoid/myeloid deregulation alone is insufficient to produce malignancy. In contrast, young Mll-AF9 mice had predominately myeloid deregulation in vivo and in vitro and developed myeloid malignancies. The early onset of distinct mixed lymphoid/myeloid lineage deregulation in Mll-AF4 mice shows evidence for both instructive" and "noninstructive" roles for AF4 and AF9 as partners in MLL fusion genes. The molecular basis for "instruction" and secondary cooperating mutations can now be studied in our Mll-AF4 model."Catalog #: Product Name: 03630 MethoCultâ„¢ M3630 Catalog #: 03630 Product Name: MethoCultâ„¢ M3630 Barbui AM et al. (APR 2006) Experimental hematology 34 4 475--85Clinical grade expansion of CD45RA, CD45RO, and CD62L-positive T-cell lines from HLA-compatible donors: high cytotoxic potential against AML and ALL cells.
OBJECTIVE: Identification of a clinical grade method for the ex vivo generation of donor-derived T cells cytotoxic against both myeloid and lymphoblastic cells still remains elusive. We investigated rapid generation and expansion of donor derived-allogeneic T-cell lines cytotoxic against patient leukemic cells. MATERIALS AND METHODS: Acute myelogenous leukemia (AML) and acute lymphoblastic leukemia (ALL) blasts were cultured 5 days in Stem Span, granulocyte macrophage colony-stimulating factor, interleukin-4, and calcium ionophore. All B-precursor ALL (N22) and AML (N13), but not T-cell ALL (N3), differentiated into mature leukemia-derived antigen-presenting cells (LD-APC). All but one LD-APC generated cytotoxic T lymphocyte (CTL) from adult human leukocyte antigen (HLA)-identical (N8) or unrelated donors (N2). RESULTS: Upon in vitro culture, donor-derived CTL acquired a memory T phenotype, showing concomitant high CD45RA, CD45RO, CD62L expression. CD8(+) cells, but not CD4(+) cells, were granzyme, perforine, and interferon-gamma-positive. Pooled CD4(+) and CD8(+) cells were cytotoxic against leukemic blasts (32%, 30:1 E:T ratio), but not against autologous or patient-derived phytohemagglutinin blasts. LD-APC from five ALL patients were used to generate CTL from cord blood. A mixed population of CD4(+) and CD8(+) cells was documented in 54% of wells. T cells acquired classical effector memory phenotype and showed a higher cytotoxicity against leukemia blasts (47%, 1:1 E:T ratio). Adult and cord blood CTL showed a skewing from a complete T-cell receptor repertoire to an oligo-clonal/clonal pattern. CONCLUSIONS: Availability of these cells should allow clinical trials for salvage treatment of leukemia patients relapsing after allogeneic stem cell transplantation.Catalog #: Product Name: 09600 StemSpanâ„¢ SFEM Catalog #: 09600 Product Name: StemSpanâ„¢ SFEM Kim S-J et al. (MAY 2006) Human molecular genetics 15 10 1580--6Palmitoyl-protein thioesterase-1 deficiency leads to the activation of caspase-9 and contributes to rapid neurodegeneration in INCL.
The infantile neuronal ceroid lipofuscinosis (INCL), a rare (one in 100 000 births) but one of the most lethal inherited neurodegenerative storage disorders of childhood, is caused by inactivating mutations in the palmitoyl-protein thioesterase-1 (PPT1) gene. PPT1 cleaves thioester linkages in s-acylated (palmitoylated) proteins and facilitates their degradation and/or recycling. Thus, PPT1-deficiency leads to an abnormal intracellular accumulation of s-acylated proteins causing INCL pathogenesis. Although neuronal apoptosis is the suggested cause of neurodegeneration in this disease, the molecular mechanism(s) remains poorly understood. We recently reported that one of the major pathways of neuronal apoptosis in PPT1-knockout (PPT1-KO) mice that mimic INCL, is mediated by endoplasmic reticulum (ER) stress-induced caspase-12 activation. ER stress also increases the production of reactive oxygen species (ROS), disrupts Ca(2+) homeostasis and increases the potential for destabilizing mitochondrial membrane. Mitochondrial membrane destabilization activates caspase-9 present in this organelle, and can mediate apoptosis. We report here that the levels of superoxide dismutase (SOD), most likely induced by ROS, in human INCL as well as PPT1-KO mouse brain tissues are markedly elevated. Moreover, we demonstrate that activated caspase-3 and cleaved-PARP, indicative of apoptosis, are also increased in these tissues. Using cultured neurospheres from PPT1-KO and wild-type mouse fetuses, we further demonstrate that the levels of ROS, SOD-2, cleaved-caspase-9, activated caspase-3 and cleaved-PARP are elevated. We propose that: (i) ER stress due to PPT1-deficiency increases ROS and disrupts calcium homeostasis activating caspase-9 and (ii) caspase-9 activation mediates caspase-3 activation and apoptosis contributing to rapid neurodegeneration in INCL.Catalog #: Product Name: 05700 NeuroCultâ„¢ Basal Medium (Mouse & Rat) 05701 NeuroCultâ„¢ Proliferation Supplement (Mouse & Rat) 05702 NeuroCultâ„¢ Proliferation Kit (Mouse & Rat) Catalog #: 05700 Product Name: NeuroCultâ„¢ Basal Medium (Mouse & Rat) Catalog #: 05701 Product Name: NeuroCultâ„¢ Proliferation Supplement (Mouse & Rat) Catalog #: 05702 Product Name: NeuroCultâ„¢ Proliferation Kit (Mouse & Rat) Zeng Z et al. ( 2006) Cancer research 66 7 3737--3746Simultaneous inhibition of PDK1/AKT and Fms-like tyrosine kinase 3 signaling by a small-molecule KP372-1 induces mitochondrial dysfunction and apoptosis in acute myelogenous leukemia.
Phosphoinositol-3-kinase (PI3K)/protein kinase B (AKT) and Fms-like tyrosine kinase 3 (FLT3) signaling are aberrantly activated in acute myelogenous leukemia (AML) cells. Constitutively activated AKT and FLT3 regulate leukemia cell survival and resistance to chemotherapy. In this study, we investigated the effects of the novel multiple kinase inhibitor KP372-1 on the survival of AML cell lines and primary AML samples. KP372-1 directly inhibited the kinase activity of AKT, PDK1, and FLT3 in a concentration-dependent manner. Western blot analysis indicated that KP372-1 decreased the phosphorylation of AKT on both Ser(473) and Thr(308); abrogated the phosphorylation of p70S6 kinase, BAD, and Foxo3a via PI3K/AKT signaling; and down-regulated expression of PIM-1 through direct inhibition of FLT3. Treatment of AML cell lines with KP372-1 resulted in rapid generation of reactive oxygen species and stimulation of oxygen consumption, followed by mitochondrial depolarization, caspase activation, and phosphatidylserine externalization. KP372-1 induced pronounced apoptosis in AML cell lines and primary samples irrespective of their FLT3 status, but not in normal CD34(+) cells. Moreover, KP372-1 markedly decreased the colony-forming ability of primary AML samples (IC(50) textless 200 nmol/L) with minimal cytotoxic effects on normal progenitor cells. Taken together, our results show that the simultaneous inhibition of critical prosurvival kinases by KP372-1 leads to mitochondrial dysfunction and apoptosis of AML but not normal hematopoietic progenitor cells.Coleman TR et al. (APR 2006) Proceedings of the National Academy of Sciences of the United States of America 103 15 5965--70Cytoprotective doses of erythropoietin or carbamylated erythropoietin have markedly different procoagulant and vasoactive activities.
Recombinant human erythropoietin (rhEPO) is receiving increasing attention as a potential therapy for prevention of injury and restoration of function in nonhematopoietic tissues. However, the minimum effective dose required to mimic and augment these normal paracrine functions of erythropoietin (EPO) in some organs (e.g., the brain) is higher than for treatment of anemia. Notably, a dose-dependent risk of adverse effects has been associated with rhEPO administration, especially in high-risk groups, including polycythemia-hyperviscosity syndrome, hypertension, and vascular thrombosis. Of note, several clinical trials employing relatively high dosages of rhEPO in oncology patients were recently halted after an increase in mortality and morbidity, primarily because of thrombotic events. We recently identified a heteromeric EPO receptor complex that mediates tissue protection and is distinct from the homodimeric receptor responsible for the support of erythropoiesis. Moreover, we developed receptor-selective ligands that provide tools to assess which receptor isoform mediates which biological consequence of rhEPO therapy. Here, we demonstrate that rhEPO administration in the rat increases systemic blood pressure, reduces regional renal blood flow, and increases platelet counts and procoagulant activities. In contrast, carbamylated rhEPO, a heteromeric receptor-specific ligand that is fully tissue protective, increases renal blood flow, promotes sodium excretion, reduces injury-induced elevation in procoagulant activity, and does not effect platelet production. These preclinical findings suggest that nonerythropoietic tissue-protective ligands, which appear to elicit fewer adverse effects, may be especially useful in clinical settings for tissue protection.Catalog #: Product Name: 04534 MethoCultâ„¢ H4534 Classic Without EPO 04564 Starter Kit for MethoCultâ„¢ H4534 Classic Without EPO Catalog #: 04534 Product Name: MethoCultâ„¢ H4534 Classic Without EPO Catalog #: 04564 Product Name: Starter Kit for MethoCultâ„¢ H4534 Classic Without EPO Jamieson CHM et al. (APR 2006) Proceedings of the National Academy of Sciences of the United States of America 103 16 6224--9The JAK2 V617F mutation occurs in hematopoietic stem cells in polycythemia vera and predisposes toward erythroid differentiation.
Although a large proportion of patients with polycythemia vera (PV) harbor a valine-to-phenylalanine mutation at amino acid 617 (V617F) in the JAK2 signaling molecule, the stage of hematopoiesis at which the mutation arises is unknown. Here we isolated and characterized hematopoietic stem cells (HSC) and myeloid progenitors from 16 PV patient samples and 14 normal individuals, testing whether the JAK2 mutation could be found at the level of stem or progenitor cells and whether the JAK2 V617F-positive cells had altered differentiation potential. In all PV samples analyzed, there were increased numbers of cells with a HSC phenotype (CD34+CD38-CD90+Lin-) compared with normal samples. Hematopoietic progenitor assays demonstrated that the differentiation potential of PV was already skewed toward the erythroid lineage at the HSC level. The JAK2 V617F mutation was detectable within HSC and their progeny in PV. Moreover, the aberrant erythroid potential of PV HSC was potently inhibited with a JAK2 inhibitor, AG490.Catalog #: Product Name: 04435 MethoCultâ„¢ H4435 Enriched Catalog #: 04435 Product Name: MethoCultâ„¢ H4435 Enriched Pirson L et al. (JUL 2006) Stem cells (Dayton, Ohio) 24 7 1814--21Despite inhibition of hematopoietic progenitor cell growth in vitro, the tyrosine kinase inhibitor imatinib does not impair engraftment of human CD133+ cells into NOD/SCIDbeta2mNull mice.
There is potential interest for combining allogeneic hematopoietic cell transplantation (HCT), and particularly allogeneic HCT with a nonmyeloablative regimen, to the tyrosine kinase inhibitor imatinib (Glivec; Novartis, Basel, Switzerland, http://www.novartis.com) in order to maximize anti-leukemic activity against Philadelphia chromosome-positive leukemias. However, because imatinib inhibits c-kit, the stem cell factor receptor, it could interfere with bone marrow engraftment. In this study, we examined the impact of imatinib on normal progenitor cell function. Imatinib decreased the colony-forming capacity of mobilized peripheral blood human CD133(+) cells but not that of long-term culture-initiating cells. Imatinib also decreased the proliferation of cytokine-stimulated CD133(+) cells but did not induce apoptosis of these cells. Expression of very late antigen (VLA)-4, VLA-5, and CXCR4 of CD133(+) cells was not modified by imatinib, but imatinib decreased the ability of CD133(+) cells to migrate. Finally, imatinib did not decrease engraftment of CD133(+) cells into irradiated nonobese diabetic/severe combined immunodeficient/beta2m(null) mice conditioned with 3 or 1 Gy total body irradiation. In summary, our results suggest that, despite inhibition of hematopoietic progenitor cell growth in vitro, imatinib does not interfere with hematopoietic stem cell engraftment.Catalog #: Product Name: 05100 MyeloCultâ„¢ H5100 04435 MethoCultâ„¢ H4435 Enriched 04970 MegaCultâ„¢-C Complete Kit Without Cytokines 04971 MegaCultâ„¢-C Complete Kit with Cytokines 04900 MegaCultâ„¢-C Medium Without Cytokines 04901 MegaCultâ„¢-C Medium with Cytokines 04960 MegaCultâ„¢-C Collagen and Medium Without Cytokines 04961 MegaCultâ„¢-C Collagen and Medium with Cytokines Catalog #: 05100 Product Name: MyeloCultâ„¢ H5100 Catalog #: 04435 Product Name: MethoCultâ„¢ H4435 Enriched Catalog #: 04970 Product Name: MegaCultâ„¢-C Complete Kit Without Cytokines Catalog #: 04971 Product Name: MegaCultâ„¢-C Complete Kit with Cytokines Catalog #: 04900 Product Name: MegaCultâ„¢-C Medium Without Cytokines Catalog #: 04901 Product Name: MegaCultâ„¢-C Medium with Cytokines Catalog #: 04960 Product Name: MegaCultâ„¢-C Collagen and Medium Without Cytokines Catalog #: 04961 Product Name: MegaCultâ„¢-C Collagen and Medium with Cytokines Maes C et al. (MAY 2006) The Journal of clinical investigation 116 5 1230--42Placental growth factor mediates mesenchymal cell development, cartilage turnover, and bone remodeling during fracture repair.
Current therapies for delayed- or nonunion bone fractures are still largely ineffective. Previous studies indicated that the VEGF homolog placental growth factor (PlGF) has a more significant role in disease than in health. Therefore we investigated the role of PlGF in a model of semi-stabilized bone fracture healing. Fracture repair in mice lacking PlGF was impaired and characterized by a massive accumulation of cartilage in the callus, reminiscent of delayed- or nonunion fractures. PlGF was required for the early recruitment of inflammatory cells and the vascularization of the fracture wound. Interestingly, however, PlGF also played a role in the subsequent stages of the repair process. Indeed in vivo and in vitro findings indicated that PlGF induced the proliferation and osteogenic differentiation of mesenchymal progenitors and stimulated cartilage turnover by particular MMPs. Later in the process, PlGF was required for the remodeling of the newly formed bone by stimulating osteoclast differentiation. As PlGF expression was increased throughout the process of bone repair and all the important cell types involved expressed its receptor VEGFR-1, the present data suggest that PlGF is required for mediating and coordinating the key aspects of fracture repair. Therefore PlGF may potentially offer therapeutic advantages for fracture repair.Catalog #: Product Name: 03434 MethoCultâ„¢ GF M3434 03334 MethoCultâ„¢ M3334 Catalog #: 03434 Product Name: MethoCultâ„¢ GF M3434 Catalog #: 03334 Product Name: MethoCultâ„¢ M3334 Items 745 to 756 of 7990 total
Shop ByFilter Results- Resource Type
-
- Reference 7990 items
- Product Type
-
- 24 items
- Area of Interest
-
- 11 items
- Angiogenic Cell Research 48 items
- Cancer 600 items
- Cell Line Development 137 items
- Chimerism 5 items
- Cord Blood Banking 23 items
- Drug Discovery and Toxicity Testing 176 items
- Endothelial Cell Biology 2 items
- Epithelial Cell Biology 156 items
- HIV 51 items
- HLA 7 items
- Immunology 733 items
- Infectious Diseases 1 item
- Neuroscience 487 items
- Stem Cell Biology 2484 items
- Transplantation Research 53 items
- Brand
-
- 0 11 items
- ALDECOUNT 7 items
- ALDEFLUOR 216 items
- AggreWell 55 items
- ArciTect 1 item
- BrainPhys 45 items
- ClonaCell 83 items
- CryoStor 65 items
- ES-Cult 74 items
- EasyPick 1 item
- EasySep 751 items
- EpiCult 12 items
- HepatiCult 1 item
- ImmunoCult 7 items
- IntestiCult 142 items
- Lymphoprep 9 items
- MammoCult 45 items
- MegaCult 33 items
- MesenCult 133 items
- MethoCult 440 items
- MyeloCult 61 items
- MyoCult 2 items
- NeuroCult 350 items
- NeuroFluor 1 item
- PancreaCult 3 items
- PneumaCult 77 items
- RSeT 6 items
- ReLeSR 1 item
- RoboSep 20 items
- RosetteSep 252 items
- STEMdiff 48 items
- STEMvision 3 items
- SepMate 29 items
- StemSpan 219 items
- TeSR 1447 items
- mFreSR 3 items
- Cell and Tissue Source
-
- 24 items
- Cell Line
-
- 24 items
- Cell Type
-
- 12 items
- Airway Cells 40 items
- B Cells 134 items
- Brain Tumor Stem Cells 81 items
- Cancer Cells and Cell Lines 116 items
- Cardiomyocytes, PSC-Derived 8 items
- Dendritic Cells 59 items
- Dermal Cells 1 item
- Endothelial Cells 1 item
- Epithelial Cells 48 items
- Granulocytes and Subsets 61 items
- Hematopoietic Stem and Progenitor Cells 765 items
- Hepatic Cells 2 items
- Hybridomas 73 items
- Innate Lymphoid Cells 3 items
- Intestinal Cells 12 items
- Leukemia/Lymphoma Cells 8 items
- Mammary Cells 68 items
- Mesenchymal Stem and Progenitor Cells 132 items
- Monocytes 105 items
- Mononuclear Cells 32 items
- Myeloid Cells 99 items
- NK Cells 79 items
- Neural Cells, PSC-Derived 17 items
- Neural Stem and Progenitor Cells 377 items
- Neurons 135 items
- Plasma 3 items
- Pluripotent Stem Cells 1676 items
- Prostate Cells 7 items
- Renal Cells 2 items
- T Cells 178 items
- T Cells, CD4+ 84 items
- T Cells, CD8+ 48 items
- T Cells, Regulatory 18 items
Loading...Copyright © 2025 º£½ÇÆÆ½â°æ. All rights reserved.