Chaoying Yin

An internal promoter underlies the difference in disease severity between N- and C-terminal truncation mutations of Titin.

p19(ARF) is dispensable for oncogenic stress-induced p53-mediated apoptosis and tumor suppression in vivo.

p53 must be competent for transcriptional regulation to suppress tumor formation.

Somatic induction of Pten loss in a preclinical astrocytoma model reveals major roles in disease progression and avenues for target discovery and validation.

Magnetic resonance angiography visualization of abnormal tumor vasculature in genetically engineered mice.

Optimization of self-complementary AAV vectors for liver-directed expression results in sustained correction of hemophilia B at low vector dose.

Apoptosis is the essential target of selective pressure against p53, whereas loss of additional p53 functions facilitates carcinoma progression.

Perturbation of Rb, p53, and Brca1 or Brca2 cooperate in inducing metastatic serous epithelial ovarian cancer.

Oversized AAV transductifon is mediated via a DNA-PKcs-independent, Rad51C-dependent repair pathway.

Evolutionary etiology of high-grade astrocytomas.

Stoichiometry of Gata4, Mef2c, and Tbx5 influences the efficiency and quality of induced cardiac myocyte reprogramming.

In vivo cardiac reprogramming using an optimal single polycistronic construct.