Ontology highlight
ABSTRACT:
INSTRUMENT(S): maXis
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Lung
DISEASE(S): Lung Cancer
SUBMITTER: Barbara Darnhofer
LAB HEAD: Ruth Birner-Gruenberger
PROVIDER: PXD007223 | Pride | 2018-09-18
REPOSITORIES: Pride
Action | DRS | |||
---|---|---|---|---|
3_10_LFQ_A549_TT_GE3_01_2714.baf | Other | |||
3_3_LFQ_A549_TT_GE1_01_2710.baf | Other | |||
3_7_LFQ_A549_TT_GE2_01_2712.baf | Other | |||
6_31_LFQ_A549_TT_GC8_01_2708.baf | Other | |||
B8_LFQ_A549_TT_GC4_01_2700.baf | Other |
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Tomin Tamara T Fritz Katarina K Gindlhuber Juergen J Waldherr Linda L Pucher Bettina B Thallinger Gerhard G GG Nomura Daniel K DK Schittmayer Matthias M Birner-Gruenberger Ruth R
Journal of proteome research 20180307 4
Adipose triglyceride lipase (ATGL) catalyzes the rate limiting step in triacylglycerol breakdown in adipocytes but is expressed in most tissues. The enzyme was shown to be lost in many human tumors, and its loss may play a role in early stages of cancer development. Here, we report that loss of ATGL supports a more-aggressive cancer phenotype in a model system in which ATGL was deleted in A549 lung cancer cells by CRISPR/Cas9. We observed that loss of ATGL led to triacylglycerol accumulation in ...[more]