Fig. 1

Structural representation, transcriptional effects and regulatory pathways of CDH1L. a Schematic representation of CHD1L protein. CHD1L encompasses four domains, SNF2 family N-terminal domain (49–328 aa, blue color) containing the ATP-binding region in N-terminal, helicase C-terminal domain (346–459 aa, blue color) containing nucleotide binding region, Selenoprotein S (SelS) (579–695 aa, pink color) consisting of several mammalian SelS sequences and a macro domain (716–866 aa, yellow color) containing ADP-ribose binding region in C-terminal. &9:Omega-N-methylarginine, no additional details recorded. DEXDc (65–205 aa):DEAD-like helicases superfamily. A diverse family of proteins involved in ATP-dependent RNA or DNA unwinding. This domain contains the ATP-binding region (74–78 aa, ATP binding site) and DEAH box (174–177 aa, putative Mg++ binding site). *: nucleotide binding region (371–374, 394–395, 421–423 aa). #: putative ADP-ribose binding sites (723–724, 741, 748, 750–751, 844, 846–848 aa). ɸ: ATP-binding sites (429, 450, 454, 457 aa). There are six putative phosphorylation sites: phospho-serine at 540, 607, 618, 628, 636 and 891 amino acids, respectively. b The transcriptional effects and regulatory pathways of CDH1L. (I) CHD1L accelerate cell cycle transition, which directly binds to the promoter regions of MDM2, P53, TCTP, ARHGEF9 and NTKL. (II) CHD1L promotes cell apoptosis death through activing caspase pathway, which enhances the phosphorylation of CREB, increases SPOCK expression and inhibits nuclear to mitochondrial translocation of Nur77. (III) CHD1L activate the transcription of Akt, METP2, TCF4 genes, leading to EMT (include invasion and metastasis). (IV) CHD1L regulates NF-κB and glycolysis pathways to facilitate cisplatin resistance