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A-549

RRID:CVCL_0023

Organism

Homo sapiens

Comments

Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: ENCODE project common cell types; tier 2. Part of: JFCR39 cancer cell line panel. Part of: KuDOS 95 cell line panel. Part of: MD Anderson Cell Lines Project. Part of: Naval Biosciences Laboratory (NBL) collection (transferred to ATCC in 1982). Part of: NCI60 cancer cell line panel. Doubling time: 22 hours (PubMed=25984343); 22.9 hours (DTP); ~40 hours (DSMZ). Microsatellite instability: Stable (MSS) (PubMed=12661003; Sanger). Omics: Acetylation analysis by proteomics. Omics: Deep antibody staining analysis. Omics: Deep exome analysis. Omics: Deep phosphoproteome analysis. Omics: Deep membrane proteome analysis. Omics: Deep proteome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: H3K4me3 ChIP-seq epigenome analysis. Omics: H3K9ac ChIP-seq epigenome analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: Proteome analysis by 2D-DE/MS. Omics: shRNA library screening. Omics: SNP array analysis. Omics: Transcriptome analysis. Omics: Virome analysis using proteomics. Misspelling: 'A594' in PubMed=18227028. Misspelling: 'A59' in PubMed=16354588. Discontinued: ATCC; CRL-7909.

Proper Citation

KCLB Cat# 10185, RRID:CVCL_0023

Category

Cancer cell line

Sex

Male

Synonyms

A 549, A549, NCI-A549, A549/ATCC, A549 ATCC, hA549

Vendor

KCLB

Cat Num

10185

Cross References

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GSM729843 GEO; GSM729844 GEO; GSM729845 GEO; GSM729846 GEO; GSM729847 GEO; GSM729848 GEO; GSM729849 GEO; GSM750779 GEO; GSM750780 GEO; GSM750788 GEO; GSM750789 GEO; GSM750791 GEO; GSM784244 GEO; GSM794260 GEO; GSM799336 GEO; GSM799399 GEO; GSM816649 GEO; GSM827464 GEO; GSM846285 GEO; GSM843439 GEO; GSM886858 GEO; GSM887923 GEO; GSM923418 GEO; GSM923420 GEO; GSM923425 GEO; GSM923432 GEO; GSM923433 GEO; GSM923435 GEO; GSM945243 GEO; GSM945244 GEO; GSM1086289 GEO; GSM1086290 GEO; GSM1153406 GEO; GSM1181254 GEO; GSM1181311 GEO; GSM1181344 GEO; GSM1181353 GEO; GSM1181354 GEO; GSM1181355 GEO; GSM1181356 GEO; GSM1181364 GEO; GSM1374385 GEO; GSM1374386 GEO; GSM1374387 GEO; GSM1557133 GEO; GSM1669589 ICLC; HTL03001 IFO; IFO50153 IGRhCellID; A549GEO IZSLER; BS TCL 101 JCRB; JCRB0076 KCB; KCB 200434YJ KCLB; 10185 LINCS; 50084 Lonza; 675 NCBI_Iran; C137 PRIDE; PXD000418 PRIDE; PXD002224 PRIDE; PXD002395 PRIDE; PXD003627 RCB; RCB0098 RCB; RCB3677 SKY/M-FISH/CGH; 2809 TKG; TKG 0184 TOKU-E; 3615 Wikidata; Q4649475

Publications that use this research resource

TP53 exon-6 truncating mutations produce separation of function isoforms with pro-tumorigenic functions.

  • Shirole NH
  • Elife
  • 2016 Oct 19

TP53 truncating mutations are common in human tumors and are thought to give rise to p53-null alleles. Here, we show that TP53 exon-6 truncating mutations occur at higher than expected frequencies and produce proteins that lack canonical p53 tumor suppressor activities but promote cancer cell proliferation, survival, and metastasis. Functionally and molecularly, these p53 mutants resemble the naturally occurring alternative p53 splice variant, p53-psi. Accordingly, these mutants can localize to the mitochondria where they promote tumor phenotypes by binding and activating the mitochondria inner pore permeability regulator, Cyclophilin D (CypD). Together, our studies reveal that TP53 exon-6 truncating mutations, contrary to current beliefs, act beyond p53 loss to promote tumorigenesis, and could inform the development of strategies to target cancers driven by these prevalent mutations.

Regulation of mTORC1 by lysosomal calcium and calmodulin.

  • Li RJ
  • Elife
  • 2016 Oct 27

Blockade of lysosomal calcium release due to lysosomal lipid accumulation has been shown to inhibit mTORC1 signaling. However, the mechanism by which lysosomal calcium regulates mTORC1 has remained undefined. Herein we report that proper lysosomal calcium release through the calcium channel TRPML1 is required for mTORC1 activation. TRPML1 depletion inhibits mTORC1 activity, while overexpression or pharmacologic activation of TRPML1 has the opposite effect. Lysosomal calcium activates mTORC1 by inducing association of calmodulin (CaM) with mTOR. Blocking the interaction between mTOR and CaM by antagonists of CaM significantly inhibits mTORC1 activity. Moreover, CaM is capable of stimulating the kinase activity of mTORC1 in a calcium-dependent manner in vitro. These results reveal that mTOR is a new type of CaM-dependent kinase, and TRPML1, lysosomal calcium and CaM play essential regulatory roles in the mTORC1 signaling pathway.

Human Adaptation of Ebola Virus during the West African Outbreak.

  • Urbanowicz RA
  • Cell
  • 2016 Nov 3

The 2013-2016 outbreak of Ebola virus (EBOV) in West Africa was the largest recorded. It began following the cross-species transmission of EBOV from an animal reservoir, most likely bats, into humans, with phylogenetic analysis revealing the co-circulation of several viral lineages. We hypothesized that this prolonged human circulation led to genomic changes that increased viral transmissibility in humans. We generated a synthetic glycoprotein (GP) construct based on the earliest reported isolate and introduced amino acid substitutions that defined viral lineages. Mutant GPs were used to generate a panel of pseudoviruses, which were used to infect different human and bat cell lines. These data revealed that specific amino acid substitutions in the EBOV GP have increased tropism for human cells, while reducing tropism for bat cells. Such increased infectivity may have enhanced the ability of EBOV to transmit among humans and contributed to the wide geographic distribution of some viral lineages.

Inactivation of oncogenic cAMP-specific phosphodiesterase 4D by miR-139-5p in response to p53 activation.

  • Cao B
  • Elife
  • 2016 Jul 7

Increasing evidence highlights the important roles of microRNAs in mediating p53's tumor suppression functions. Here, we report miR-139-5p as another new p53 microRNA target. p53 induced the transcription of miR-139-5p, which in turn suppressed the protein levels of phosphodiesterase 4D (PDE4D), an oncogenic protein involved in multiple tumor promoting processes. Knockdown of p53 reversed these effects. Also, overexpression of miR-139-5p decreased PDE4D levels and increased cellular cAMP levels, leading to BIM-mediated cell growth arrest. Furthermore, our analysis of human colorectal tumor specimens revealed significant inverse correlation between the expression of miR-139-5p and that of PDE4D. Finally, overexpression of miR-139-5p suppressed the growth of xenograft tumors, accompanied by decrease in PDE4D and increase in BIM. These results demonstrate that p53 inactivates oncogenic PDE4D by inducing the expression of miR-139-5p.