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- 详细信息
- 文献和实验
- 技术资料
- 英文名:
DMS114
- 库存:
1x10^6/瓶/支
- 供应商:
上海酶研
- 肿瘤类型:
详询
- 细胞类型:
小细胞肺癌细胞
- ATCC Number:
详询
- 品系:
DMS114
- 组织来源:
小细胞肺癌细胞
- 相关疾病:
DMS114
- 物种来源:
哺乳动物
- 免疫类型:
详询
- 细胞形态:
贴壁/悬浮
- 是否是肿瘤细胞:
详询
- 器官来源:
小细胞肺癌细胞
- 运输方式:
顺丰快递
- 年限:
5年
- 生长状态:
生长良好
DMS114/DMS114细胞系/DMS114细胞株/DMS114小细胞肺癌细胞
Cell line name DMS 114
Synonyms DMS-114; DMS114; Darmouth Medical School 114
Accession CVCL_1174
Resource Identification Initiative To cite this cell line use: DMS 114 (RRID:CVCL_1174)
Comments Part of: Cancer Dependency Map project (DepMap) (includes Cancer Cell Line Encyclopedia - CCLE).
Part of: COSMIC cell lines project.
Part of: FGFR genetic alteration cell panel (ATCC TCP-1034).
Part of: JFCR39 cancer cell line panel.
Part of: KuDOS 95 cell line panel.
Population: Caucasian.
Doubling time: 3.8 days (PubMed=6266631); 1.6 days (PubMed=2986244); 27 hours (PubMed=7718330).
Microsatellite instability: Stable (MSS) (Sanger).
Omics: Deep exome analysis.
Omics: Deep proteome analysis.
Omics: Deep quantitative proteome analysis.
Omics: DNA methylation analysis.
Omics: Protein expression by reverse-phase protein arrays.
Omics: SNP array analysis.
Omics: Transcriptome analysis by microarray.
Omics: Transcriptome analysis by RNAseq.
Caution: Originally classified as originating from a lung small cell carcinoma, but is reclassified as a thoracic SMARCA4-deficient undifferentiated tumor based on a number of criteria (PubMed=38180245).
Derived from site: In situ; Lung; UBERON=UBERON_0002048.
PubMed=7718330; DOI=10.1016/0959-8049(94)00472-H
Baguley B.C., Marshall E.S., Whittaker J.R., Dotchin M.C., Nixon J., McCrystal M.R., Finlay G.J., Matthews J.H.L., Holdaway K.M., van Zijl P.L.
Resistance mechanisms determining the in vitro sensitivity to paclitaxel of tumour cells cultured from patients with ovarian cancer.
Eur. J. Cancer 31A:230-237(1995)
PubMed=9212023; DOI=10.1016/S0360-3016(97)00245-9
Krarup M., Poulsen H.S., Spang-Thomsen M.
Cellular radiosensitivity of small-cell lung cancer cell lines.
Int. J. Radiat. Oncol. Biol. Phys. 38:191-196(1997)
PubMed=9744504; DOI=10.1038/bjc.1998.553; PMCID=PMC2063065
Damstrup L., Voldborg B.G.R., Spang-Thomsen M., Brunner N., Poulsen H.S.
In vitro invasion of small-cell lung cancer cell lines correlates with expression of epidermal growth factor receptor.
Br. J. Cancer 78:631-640(1998)
PubMed=12712436; DOI=10.1002/ijc.11106
Hansen L.T., Lundin C., Spang-Thomsen M., Petersen L.N., Helleday T.
The role of RAD51 in etoposide (VP16) resistance in small cell lung cancer.
Int. J. Cancer 105:472-479(2003)
PubMed=15900046; DOI=10.1093/jnci/dji133
Mashima T., Oh-hara T., Sato S., Mochizuki M., Sugimoto Y., Yamazaki K., Hamada J.-i., Tada M., Moriuchi T., Ishikawa Y., Kato Y., Tomoda H., Yamori T., Tsuruo T.
p53-defective tumors with a functional apoptosome-mediated pathway: a new therapeutic target.
J. Natl. Cancer Inst. 97:765-777(2005)
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=20215515; DOI=10.1158/0008-5472.CAN-09-3458; PMCID=PMC2881662
Rothenberg S.M., Mohapatra G., Rivera M.N., Winokur D., Greninger P., Nitta M., Sadow P.M., Sooriyakumar G., Brannigan B.W., Ulman M.J., Perera R.M., Wang R., Tam A., Ma X.-J., Erlander M., Sgroi D.C., Rocco J.W., Lingen M.W., Cohen E.E.W., Louis D.N., Settleman J., Haber D.A.
A genome-wide screen for microdeletions reveals disruption of polarity complex genes in diverse human cancers.
Cancer Res. 70:2158-2164(2010)
PubMed=22336246; DOI=10.1016/j.bmc.2012.01.017
Kong D.-X., Yamori T.
JFCR39, a panel of 39 human cancer cell lines, and its application in the discovery and development of anticancer drugs.
Bioorg. Med. Chem. 20:1947-1951(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.
Nature!中美学者共同破译粘附类 GPCR 自激活机制之谜
activation of adhesion GPCRs 工作中,研究者们回答了这一未解谜题。 孙金鹏教授团队解析了粘附类受体 GPR133 和 GPR114 结构,发现 GPR133 GPS 位点发生水解,在质膜上发生 NTF-CTF 分离,GPR114 不发生自水解,能够感知机械力。通过功能实验证明了受体感知机械力后通过 Stachel 序列激活受体,并确定 Stachel 中的 5 个疏水氨基酸组成的保守 HIM(Fss-03xφφφxφss-09),其在 Stachel 序列与受体相互作用中起着核心
同日 4 篇 Nature!中美学者共同破译粘附类 GPCR 自激活机制之谜
力,刺激驱动着细胞的动态以及机体的正常生长运行。Stachel 序列介导的 aGPCR 激活作用一直是 aGPCR 信号和功能的核心内容,Stachel 序列如何与受体作用,调控受体激活状态的通用机制仍未明晰。在 Structural basis for the tethered peptide activation of adhesion GPCRs 工作中,研究者们回答了这一未解谜题。 孙金鹏教授团队解析了粘附类受体 GPR133 和 GPR114 结构,发现 GPR133 GPS 位点发生
Triton X-114,2% 95 100 NP-40,1% 95 91 Brij*-35,1% 99 97
技术资料






