Disease relevance of TFCP2L1

• A yeast one-hybrid screen of 2.4 x 10(6) cDNA clones from human placental JEG-3 cells yielded two unique clones; one is the previously described transcription factor LBP-1b, which is induced by HIV, type I infection of lymphocytes, and the other is a new factor, termed LBP-9, that shares 83% amino acid sequence identity with LBP-1b [1].

High impact information on TFCP2L1

• Reverse transcriptase-polymerase chain reaction detected LBP-1b in human placental JEG-3, adrenal NCI-H295A, liver HepG2, cervical HeLa, and monkey kidney COS-1 cells, but LBP-9 was detected only in JEG-3 cells [1].
• Glutathione-S-transferase pull-down assays, bandshifts, and transient transfection assays showed that TReP-132 (another factor that can bind to -155/-131) does not interact with either LBP-1b or LBP-9, or influence their ability to induce or suppress transcription from the -155/-131 element [2].
• In transient transfection assays, LBP-1b activated the -155/-131 element whereas LBP-9 suppressed its LBP-1b-stimulated expression [2].
• We previously cloned two transcription factors, long terminal repeat binding protein (LBP)-1b and LBP-9, from JEG-3 cells [2].
• Gal4 transactivation assays showed that transcriptional repression activity by LBP-9 requires residues 100-200 [2].

Biological context of TFCP2L1

• Consistent and marked downregulation of TFCP2L1 was identified as one of the main mechanisms contributing to CRYAB gene silencing in ATCs [3].

Anatomical context of TFCP2L1

• All cell lines stably expressing a fusion protein of LBP-1b and enhanced green fluorescent protein increased P450scc expression, but cell lines stably expressing LBP-9 fused to enhanced green fluorescent protein either increased or decreased P450scc expression [2].

References