Hao Yang Lim

Mr. Hao Yang Lim

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Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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6 February 2025 in Cells
Verified
Journal Article
Open access
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JIJan Nikolas Iversen
Jan Nikolas Iversen
YTYee Kit Tai
Yee Kit Tai
KWKwan Yu Wu
Kwan Yu Wu
CWCraig Wong
Craig Wong
HLHao Yang Lim
Hao Yang Lim
Alfredo Franco-ObregónAlfredo Franco-Obregón
Alfredo Franco-Obregón
The cryptochromes are flavoproteins that either individually or synergistically respond to light and magnetic field directionality as well as are implicated in circadian rhythm entrainment and development. Single brief exposures (10 min) to low energy (1.5 mT) pulsed electromagnetic fields (PEMFs) were previously shown to enhance myogenesis by stimulating transient receptor potential canonical 1 (TRPC1)-mediated Ca2+ entry, whereby downwardly directed fields produced greater myogenic enhancement than upwardly directed fields. Here, we show that growth in the dark results in myoblasts losing their sensitivity to both magnetic field exposure and directionality. By contrast, overexpressing or silencing cryptochrome circadian regulator 2 (CRY2) in myoblasts enhances or reduces PEMF responses, respectively, under conditions of ambient light. Reducing cellular flavin adenine dinucleotide (FAD) content by silencing riboflavin kinase (RFK) attenuated responsiveness to PEMFs and inhibited selectivity for magnetic field direction. The upregulation of TRPC1 and cell cycle regulatory proteins typically observed in response to PEMF exposure was instead attenuated by upwardly directed magnetic fields, growth in the darkness, magnetic shielding, or the silencing of CRY2 or RFK. A physical interaction between CRY2 and TRPC1 was detected using coimmunoprecipitation and immunofluorescence, revealing their co-translocation into the nucleus after PEMF exposure. These results implicate CRY2 in an identified TRPC1-dependent magnetotransduction myogenic cascade.