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T25
SUP-T1/SUP-T1细胞系/SUP-T1细胞株/SUP-T1人T淋巴瘤细胞
Cell line name SUP-T1
Synonyms Sup-T1; SUPT-1; SupT-1; Sup T-1; SUP T-1; SUP T1; Sup T1; SupT1; SUPT1; Tsup-1; VB; Stanford University Pediatric T-cell line 1
Accession CVCL_1714
Resource Identification Initiative To cite this cell line use: SUP-T1 (RRID:CVCL_1714)
Comments Part of: Cancer Dependency Map project (DepMap) (includes Cancer Cell Line Encyclopedia - CCLE).
Part of: COSMIC cell lines project.
Population: Caucasian.
Characteristics: Has chromosomal translocations involving the genes for the alpha and beta subunits of TCR thus preventing surface expression of the endogenous TCR complex.
Virology: Useful for studies of cell fusion and cytopathic effects of HIV-1 as well as cytopathic isolates of HIV-2.
Virology: Susceptible to infection by herpesvirus 6B (HHV-6B) strain Z29 (PubMed=29304865).
Doubling time: 28 hours (PubMed=3004618); ~30 hours (DSMZ=ACC-140); ~24-36 hours (BEI_Resources=ARP-100).
Microsatellite instability: Stable (MSS) (Sanger).
Microsatellite instability: Instable (MSI) (PubMed=31068700).
Omics: Deep exome analysis.
Omics: Deep quantitative proteome analysis.
Omics: DNA methylation analysis.
Omics: SNP array analysis.
Omics: Transcriptome analysis by microarray.
Omics: Transcriptome analysis by RNAseq.
Omics: Virome analysis using RNAseq.
Derived from site: In situ; Pleural effusion; UBERON=UBERON_0000175.
Cell type: T-cell; CL=CL_0000084.
PubMed=3107838; DOI=10.1016/0092-8674(87)90542-3
Stein B.S., Gowda S.D., Lifson J.D., Penhallow R.C., Bensch K.G., Engleman E.G.
pH-independent HIV entry into CD4-positive T cells via virus envelope fusion to the plasma membrane.
Cell 49:659-668(1987)
PubMed=7849311; DOI=10.1182/blood.V85.4.893.bloodjournal854893
Stranks G., Height S.E., Mitchell P., Jadayel D.M., Yuille M.A.R., De Lord C.F.M., Clutterbuck R.D., Treleaven J.G., Powles R.L., Nacheva E., Oscier D.G., Karpas A., Lenoir G.M., Smith S.D., Millar J.L., Catovsky D., Dyer M.J.S.
Deletions and rearrangement of CDKN2 in lymphoid malignancy.
Blood 85:893-901(1995)
PubMed=8558920
Dirks W.G., Zaborski M., Jager K., Challier C., Shiota M., Quentmeier H., Drexler H.G.
The (2;5)(p23;q35) translocation in cell lines derived from malignant lymphomas: absence of t(2;5) in Hodgkin-analogous cell lines.
Leukemia 10:142-149(1996)
PubMed=9933131; DOI=10.1016/S0145-2126(98)00133-7
Burger R., Hansen-Hagge T.E., Drexler H.G., Gramatzki M.
Heterogeneity of T-acute lymphoblastic leukemia (T-ALL) cell lines: suggestion for classification by immunophenotype and T-cell receptor studies.
Leuk. Res. 23:19-27(1999)
DOI=10.1016/B978-0-12-221970-2.50457-5
Drexler H.G.
The leukemia-lymphoma cell line factsbook.
(In book) ISBN 9780122219702; pp.1-733; Academic Press; London; United Kingdom (2001)
PubMed=11264379; DOI=10.1128/JVI.75.8.3903-3915.2001; PMCID=PMC114881
Means R.E., Matthews T., Hoxie J.A., Malim M.H., Kodama T., Desrosiers R.C.
Ability of the V3 loop of serve as a target for antibody-mediated neutralization: correlation of neutralization sensitivity, growth in macrophages, and decreased dependence on CD4.
J. Virol. 75:3903-3915(2001)
PubMed=17170727; DOI=10.1038/sj.leu.2404486
Sandberg Y., Verhaaf B., van Gastel-Mol E.J., Wolvers-Tettero I.L.M., De Vos J., MacLeod R.A.F., Noordzij J.G., Dik W.A., van Dongen J.J.M., Langerak A.W.
Human T-cell lines with well-defined T-cell receptor gene rearrangements as controls for the BIOMED-2 multiplex polymerase chain reaction tubes.
Leukemia 21:230-237(2007)
PubMed=20164919; DOI=10.1038/nature08768; PMCID=PMC3145113
Bignell G.R., Greenman C.D., Davies H.R., Butler A.P., Edkins S., Andrews J.M., Buck G., Chen L., Beare D., Latimer C., Widaa S., Hinton J., Fahey C., Fu B.-Y., Swamy S., Dalgliesh G.L., Teh B.T., Deloukas P., Yang F.-T., Campbell P.J., Futreal P.A., Stratton M.R.
Signatures of mutation and selection in the cancer genome.
Nature 463:893-898(2010)
PubMed=22292511; DOI=10.2174/187221512799303172
Ho P., Dai K.-S., Chen H.-L.
Molecular cloning of a novel PPEF-1 gene variant from a T-cell lymphoblastic lymphoma cell line.
Recent Pat. DNA Gene Seq. 6:72-77(2012)
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文献和实验*发表【中文论文】请标注:由上海酶研生物科技有限公司提供;
*发表【英文论文】请标注:From Shanghai EK-Bioscience Biotechnology Co., Ltd.
喝完「无糖饮料」还想吃甜食?原来人们对糖的渴望,无法被甜味剂替代,答案都在肠道里!
1r3 和 Slc5a1 共存在于 19.6% 的细胞中。 那么,迷走神经对糖或甜味剂的反应是否由上皮 SGLT 或 T1R3 介导的呢?研究人员使用 SGLT 抑制剂 phloridzin,发现抑制 SGLT 后并不影响对三氯蔗糖的反应。相反,阻断包括 T1R3 在内的甜味受体消除了对三氯蔗糖的迷走神经反应,但不影响对蔗糖或 α-MGP 的反应。 在舌头上的味觉转导中,蔗糖和三氯蔗糖都可以激活 T1R2/T1R3 受体。但是,以上结果表明,在肠道中只有三氯蔗糖能引起味觉受体介导的迷走神经反应。这种
系从 RNA与 DNA(单链)间的杂种双链分子的形成速度,来分析某一细胞或组织中的 RNA,是由基因组 DNA哪一部分转录来的一种方法。与分析单链 DNA间形成双链分子的速度的 COt分析相对应,而将这个 RNA- DNA间的分析称为 ROt分析( RNA- COt之意)。一般使用放射性同位素标记的 DNA在 RNA过剩的条件下进行结合反应( RNA drivenhybridization)。因 RNA过剩而 DNA浓度( D)非常低,所以 DNA- DNA的结合可以忽略
「少吃」真的可以帮助杀死癌细胞!模拟禁食可重塑机体免疫,提高癌症免疫治疗的效果
免疫反应,并可减少其副作用。 禁食模拟饮食可以作用于肿瘤微环境,增加了低免疫原性的三阴性乳腺肿瘤(TNBC)中免疫治疗(抗 PD-L1 和抗 OX40)的效果。此外,FMD 还可以通过阻止免疫反应的过度激活,减少免疫相关不良事件(irAEs)的发生。 图片来源:Cell Reports 主要研究内容 禁食模拟饮食联合抗 OX40/抗 PD-L1 可阻止乳腺癌的进展 首先,研究人员将 4T1 乳腺癌细胞原位植入小鼠乳腺脂肪垫,然后用抗 OX40/抗 PD-L1 单独或联合治疗,并设置禁食模拟饮食
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