trp channels br Materials and methods br Author disclosure

Materials and methods
Author disclosure statement
Acknowledgments This study was supported by fund from National Medical Research Council (NMRC) of Singapore, the Translational Clinical Research (TCR) award (NMRC/TCR/013-NNI/2014) and STaR award (NMRC/STaR/014/2013). We thank Ms. Fiona Setiawan for collecting the patient blood samples.
Resource table. Resource details The study was approved by the Singhealth ethics committee (protocol number SHSIBC-2014-031), and written informed consent was obtained from the patient. 2ml of peripheral blood sample was obtained from a female 72-year-old Parkinson\'s disease patient carrying a heterozygous R1398H variant in LRRK2 gene. LRRK2 R1398H variant may protect the susceptibility of PD disease among Asian population (Nixon-Abell et al., 2016; Peeraully and Tan, 2012; Tan et al., 2010). PD-BP26-iPSC lines were derived using CytoTune®-iPS 2.0 Reprogramming System (Thermo Fisher Scientific), which carrying the 4 Yamanaka reprogramming factors OCT4, SOX2, cMYC and KLF4(Ban et al., 2011). This reprogramming followed the previous published protocol (Tan et al., 2014). The derived hiPSC lines displayed a typical round shape ESC-like morphology with small and tightly packed cells, and a high nucleus/cytoplasm ratio and prominent nucleoli (Fig. 1A). The presence of the R1398H variant was confirmed in hiPSC lines by Sanger sequencing (Fig. 1B), and the trp channels of pluripotency markers was verified by immunofluorescence staining (Fig. 1C). Moreover, the absence of exogenous reprogramming transgenes was observed by RT-PCR after 5–8 passages (Fig. 1D). The differentiation capacity of hiPSC lines into three germ layers was demonstrated by in vivo teratoma formation assay (Fig. 1E). The derived hiPSC lines showed normal karyotype (46, XX) (Fig. 1F).
Materials and methods
Author disclosure statement
Acknowledgments This study was supported by fund from National Medical Research Council (NMRC) of Singapore, the Translational Clinical Research (TCR) award (NMRC/TCR/013-NNI/2014) and STaR award (NMRC/STaR/014/2013). We thank Ms. Fiona Setiawan for collecting the patient blood samples.
Resource table. Resource details The study was approved by the Singhealth ethics committee (protocol number SHSIBC-2014-031), and written informed consent was obtained from the patient. 2ml of peripheral blood sample was obtained from a male 64-year-old Parkinson\'s disease patient carrying a heterozygous N551K variant in LRRK2 gene. LRRK2 N551K variant may lower the susceptibility of PD among Asian population (Peeraully and Tan, 2012; Ross et al., 2011; Tan et al., 2010). PD-BP15-iPSC lines were derived using CytoTune®-iPS 2.0 Reprogramming System (Thermo Fisher Scientific), which carrying the 4 Yamanaka reprogramming factors OCT4, SOX2, cMYC and KLF4 (Ban et al., 2011). This reprogramming followed the previous published protocol (Tan et al., 2014). The derived hiPSC lines displayed a typical round shape ESC-like morphology with small and tightly packed cells, and a high nucleus/cytoplasm ratio and prominent nucleoli (Fig. 1A). The presence of the N551K variant was confirmed in hiPSC lines by sanger sequencing (Fig. 1B), and the expression of pluripotency markers was verified by immunofluorescence staining (Fig. 1C). Moreover, the absence of exogenous reprogramming transgenes was observed by RT-PCR after 5–8 passages (Fig. 1D). The differentiation capacity of hiPSC lines into three germ layers was demonstrated by in vivo teratoma formation assay (Fig. 1E). The derived hiPSC lines showed normal karyotype (46, XY) (Fig. 1F).
Materials and methods
Author disclosure statement
Acknowledgments This study was supported by fund from National Medical Research Council (NMRC) of Singapore, the Translational Clinical Research (TCR) award (NMRC/TCR/013-NNI/2014) and STaR award (NMRC/STaR/014/2013). We thank Ms. Fiona Setiawan for collecting the patient blood samples.