Yongzheng He
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View article: A proteasome-resistant fragment of NIK mediates oncogenic NF-κB signaling in schwannomas
A proteasome-resistant fragment of NIK mediates oncogenic NF-κB signaling in schwannomas Open
Schwannomas are common, highly morbid and medically untreatable tumors that can arise in patients with germ line as well as somatic mutations in neurofibromatosis type 2 (NF2). These mutations most commonly result in the loss of function o…
View article: Cabozantinib for neurofibromatosis type 1–related plexiform neurofibromas: a phase 2 trial
Cabozantinib for neurofibromatosis type 1–related plexiform neurofibromas: a phase 2 trial Open
View article: Respiratory Syncytial Virus Risk Profile in Hospitalized Infants and Comparison with Influenza and COVID-19 Controls in Valladolid, Spain, 2010–2022
Respiratory Syncytial Virus Risk Profile in Hospitalized Infants and Comparison with Influenza and COVID-19 Controls in Valladolid, Spain, 2010–2022 Open
View article: RSV Risk Profile in Hospitalized Adults and Comparison with Influenza and COVID-19 Controls in Valladolid, Spain, 2010–2022
RSV Risk Profile in Hospitalized Adults and Comparison with Influenza and COVID-19 Controls in Valladolid, Spain, 2010–2022 Open
RSV especially affects those with comorbidities, coinfections, and living in care institutions. RSV vaccination could have an important public health impact in this population.
View article: Clostridium butyricum regulates intestinal barrier function via trek1 to improve behavioral abnormalities in mice with autism spectrum disorder
Clostridium butyricum regulates intestinal barrier function via trek1 to improve behavioral abnormalities in mice with autism spectrum disorder Open
View article: Brigatinib causes tumor shrinkage in both NF2-deficient meningioma and schwannoma through inhibition of multiple tyrosine kinases but not ALK
Brigatinib causes tumor shrinkage in both NF2-deficient meningioma and schwannoma through inhibition of multiple tyrosine kinases but not ALK Open
Neurofibromatosis Type 2 (NF2) is an autosomal dominant genetic syndrome caused by mutations in the NF2 tumor suppressor gene resulting in multiple schwannomas and meningiomas. There are no FDA approved therapies for these tumors and their…
View article: Cabozantinib for neurofibromatosis type 1–related plexiform neurofibromas: a phase 2 trial
Cabozantinib for neurofibromatosis type 1–related plexiform neurofibromas: a phase 2 trial Open
View article: Characterization of the Tumor Microenvironment of Neurofibromatosis Type I Plexiform Neurofibromas
Characterization of the Tumor Microenvironment of Neurofibromatosis Type I Plexiform Neurofibromas Open
Background/Objective: Neurofibromatosis type 1 (NF1) is a cancer predisposition syndrome caused by mutations in the NF1 tumor suppressor gene. Patients with NF1 develop tumors of the peripheral nervous system called plexiform neurofibromas…
View article: Correction: Genetic disruption of the small GTPase RAC1 prevents plexiform neurofibroma formation in mice with neurofibromatosis type 17
Correction: Genetic disruption of the small GTPase RAC1 prevents plexiform neurofibroma formation in mice with neurofibromatosis type 17 Open
View article: Schwannoma development is mediated by Hippo pathway dysregulation and modified by RAS/MAPK signaling
Schwannoma development is mediated by Hippo pathway dysregulation and modified by RAS/MAPK signaling Open
Schwannomas are tumors of the Schwann cells that cause chronic pain, numbness, and potentially life-threatening impairment of vital organs. Despite the identification of causative genes, including NF2 (Merlin), INI1/SMARCB1, and LZTR1, the…
View article: Genetic disruption of the small GTPase RAC1 prevents plexiform neurofibroma formation in mice with neurofibromatosis type 17
Genetic disruption of the small GTPase RAC1 prevents plexiform neurofibroma formation in mice with neurofibromatosis type 17 Open
View article: Cdkn2a (Arf) loss drives NF1-associated atypical neurofibroma and malignant transformation
Cdkn2a (Arf) loss drives NF1-associated atypical neurofibroma and malignant transformation Open
Plexiform neurofibroma (PN) tumors are a hallmark manifestation of neurofibromatosis type 1 (NF1) that arise in the Schwann cell (SC) lineage. NF1 is a common heritable cancer predisposition syndrome caused by germline mutations in the NF1…
View article: EXTH-13. REDUCTION OF TUMOR BURDEN AND HEARING LOSS WITH A MULTIPLE RECEPTOR TYROSINE KINASE INHIBITOR BRIGATINIB IN A GENETICALLY ENGINEERED MOUSE MODEL OF NEUROFIBROMATOSIS TYPE 2
EXTH-13. REDUCTION OF TUMOR BURDEN AND HEARING LOSS WITH A MULTIPLE RECEPTOR TYROSINE KINASE INHIBITOR BRIGATINIB IN A GENETICALLY ENGINEERED MOUSE MODEL OF NEUROFIBROMATOSIS TYPE 2 Open
Neurofibromatosis Type 2 (NF2) is an autosomal dominant genetic disorder caused by germline mutations in the tumor suppressor gene NF2, which encodes the protein Merlin. Patients with NF2 may develop bilateral vestibular schwannomas, which…
View article: A proteasome-resistant fragment of NIK mediates oncogenic NF-κB signaling in schwannomas
A proteasome-resistant fragment of NIK mediates oncogenic NF-κB signaling in schwannomas Open
Schwannomas are common, highly morbid and medically untreatable tumors that can arise in patients with germ line as well as somatic mutations in neurofibromatosis type 2 (NF2). These mutations most commonly result in the loss of function o…
View article: Chemopreventative celecoxib fails to prevent schwannoma formation or sensorineural hearing loss in genetically engineered murine model of neurofibromatosis type 2
Chemopreventative celecoxib fails to prevent schwannoma formation or sensorineural hearing loss in genetically engineered murine model of neurofibromatosis type 2 Open
Mutations in the tumor suppressor gene NF2 lead to Neurofibromatosis type 2 (NF2), a tumor predisposition syndrome characterized by the development of schwannomas, including bilateral vestibular schwannomas with complete penetrance.…
View article: Improving Combination Osteoporosis Therapy in a Preclinical Model of Heightened Osteoanabolism
Improving Combination Osteoporosis Therapy in a Preclinical Model of Heightened Osteoanabolism Open
Combining anticatabolic agents with parathyroid hormone (PTH) to enhance bone mass has yielded mixed results in osteoporosis patients. Toward the goal of enhancing the efficacy of these regimens, we tested their utility in combination with…
View article: An abnormal bone marrow microenvironment contributes to hematopoietic dysfunction in Fanconi anemia
An abnormal bone marrow microenvironment contributes to hematopoietic dysfunction in Fanconi anemia Open
Fanconi anemia is a complex heterogeneous genetic disorder with a high incidence of bone marrow failure, clonal evolution to acute myeloid leukemia and mesenchymal-derived congenital anomalies. Increasing evidence in Fanconi anemia and oth…
View article: ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis
ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis Open
Asxl1 loss–induced myeloid malignancies are mediated partially through impaired ASXL1 cohesin interaction and cohesin functions.
View article: Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cells, Leading to Bohring-Opitz-like Syndrome in Mice
Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cells, Leading to Bohring-Opitz-like Syndrome in Mice Open
De novo ASXL1 mutations are found in patients with Bohring-Opitz syndrome, a disease with severe developmental defects and early childhood mortality. The underlying pathologic mechanisms remain largely unknown. Using Asxl1-targeted murine …
View article: Genome-Wide Mapping and Interrogation of the Nmp4 Antianabolic Bone Axis
Genome-Wide Mapping and Interrogation of the Nmp4 Antianabolic Bone Axis Open
PTH is an osteoanabolic for treating osteoporosis but its potency wanes. Disabling the transcription factor nuclear matrix protein 4 (Nmp4) in healthy, ovary-intact mice enhances bone response to PTH and bone morphogenetic protein 2 and pr…
View article: Hyperactive RAS/PI3-K/MAPK Signaling Cascade in Migration and Adhesion of Nf1 Haploinsufficient Mesenchymal Stem/Progenitor Cells
Hyperactive RAS/PI3-K/MAPK Signaling Cascade in Migration and Adhesion of Nf1 Haploinsufficient Mesenchymal Stem/Progenitor Cells Open
Neurofibromatosis type 1 (NF1) is an autosomal dominant disease caused by mutations in the NF1 tumor suppressor gene, which affect approximately 1 out of 3000 individuals. Patients with NF1 suffer from a range of malignant and nonmalignant…
View article: Hyperactive RAS/PI3-K/MAPK Signaling Cascade in Migration and Adhesion of Nf1 Haploinsufficient Mesenchymal Stem/Progenitor Cells
Hyperactive RAS/PI3-K/MAPK Signaling Cascade in Migration and Adhesion of Nf1 Haploinsufficient Mesenchymal Stem/Progenitor Cells Open
Neurofibromatosis type 1 (NF1) is an autosomal dominant disease caused by mutations in the NF1 tumor suppressor gene, which affect approximately 1 out of 3000 individuals. Patients with NF1 suffer from a range of malignant and nonmalignant…
View article: <i>Nf1</i> Haploinsufficiency Alters Myeloid Lineage Commitment and Function, Leading to Deranged Skeletal Homeostasis
<i>Nf1</i> Haploinsufficiency Alters Myeloid Lineage Commitment and Function, Leading to Deranged Skeletal Homeostasis Open
Although nullizygous loss of NF1 leads to myeloid malignancies, haploinsufficient loss of NF1 (Nf1) has been shown to contribute to osteopenia and osteoporosis which occurs in approximately 50% of neurofibromatosis type 1 (NF1) patients. B…