A5086249183- Cleft Lip and Palate Research
- Craniofacial Disorders and Treatments
- Epigenetics and DNA Methylation
- Developmental Biology and Gene Regulation
- Folate and B Vitamins Research
- Neurogenesis and neuroplasticity mechanisms
- Hedgehog Signaling Pathway Studies
- Congenital Ear and Nasal Anomalies
- Olfactory and Sensory Function Studies
- Wnt/β-catenin signaling in development and cancer
- Nerve injury and regeneration
- Genetics and Neurodevelopmental Disorders
- Congenital Anomalies and Fetal Surgery
- dental development and anomalies
- Urological Disorders and Treatments
- Pluripotent Stem Cells Research
- Cancer-related gene regulation
- Cancer-related molecular mechanisms research
- Kruppel-like factors research
- Autism Spectrum Disorder Research
- MicroRNA in disease regulation
- Tracheal and airway disorders
- Congenital heart defects research
- Head and Neck Surgical Oncology
University of California, Davis
2019-2023
Shriners Hospitals for Children - Erie
2019-2023
Shriners Hospitals for Children - Northern California
2020-2023
Formation of highly unique and complex facial structures is controlled by genetic programs that are responsible for the precise coordination three-dimensional tissue morphogenesis. However, underlying mechanisms governing these processes remain poorly understood. We combined mouse genomic approaches to define normal defective midfacial Conditional inactivation Wnt secretion protein Wls in Pax3-expressing lineage cells disrupted frontonasal primordial patterning, cell survival directional...
Neural tube defects (NTDs) are among the common and severe birth with poorly understood etiology. Mutations in Wnt co-receptor LRP6 associated NTDs humans. Either gain-of-function (GOF) or loss-of-function (LOF) mutations of Lrp6 can cause mice. Lrp6-GOF mutants may be attributed to altered β-catenin-independent noncanonical signaling. However, mechanisms underlying Lrp6-LOF role Lrp6-mediated canonical Wnt/β-catenin signaling neural closure remain unresolved. We previously demonstrated that...
Abstract Cranial neural crest (NC) cells migrate long distances to populate the future craniofacial regions and give rise various tissues, including facial cartilage, bones, connective cranial nerves. However, mechanism that drives fate determination of NC remains unclear. Using single-cell RNA sequencing combined genetic mapping, we reconstructed developmental trajectories cells, traced their differentiation in mouse embryos. We identified four major cell lineages at different status:...
The secondary palate forms from two lateral primordia called the palatal shelves which form a contact in midline, become adherent at fusing interface (medial edge epithelia, MEE) and subsequently fuse. gene encoding transforming growth factor-ß3 ( Tgfb3 ) is strongly specifically expressed MEE cells. Our previous study suggested that expression controlled via upstream cis-regulatory elements around neighboring Ift43 gene. Another canonical Wnt signaling ß-Catenin responsible for MEE-specific...
Abstract Background In addition to genomic risk variants and environmental influences, increasing evidence suggests epigenetic modifications are important for orofacial development their alterations can contribute clefts. Ezh2 encodes a core catalytic component of the Polycomb repressive complex responsible methyl marks Histone H3 as mechanism repressing target genes. The role in clefts remains unknown. Aims To investigate epithelial Ezh2‐dependent methylation secondary palatogenesis....