Genetics and Diseases

illustration of cytoplasm2

All documents are PDF. If needed, you can download Adobe reader here. Adobe Reader logo

CNBP regulates forebrain formation at organogenesis stage in chick embryos

 

Haploinsuffciency for Znf9 in Znf9+/− Mice Is Associated with Multiorgan Abnormalities Resembling Myotonic Dystrophy

 

The Triple Functions of D2 Silencing in Treatment of Periapical Disease

 

C1 Silencing Attenuates Inflammation and Alveolar Bone Resorption in Endodontic Disease

 

Molecular cloning, developmental expression, promoter analysis and functional characterization of the mouse CNBP gene

 

Bone resorption deficiency affects tooth root development in RANKL mutant mice due to attenuated IGF-1 signaling in radicular odontoblasts

 

The zinc-finger protein CNBP is required for forebrain formation in the mouse

 

Inhibition of Rgs10 Expression Prevents Immune Cell Infiltration in Bacteria-induced Inflammatory Lesions and Osteoclast-mediated Bone Destruction

 

TRAF Family Member-Associated NF-κB Activator (TANK) Induced by RANKL Negatively Regulates Osteoclasts Survival and Function

 

Silencing of Atp6v1c1 Prevents Breast Cancer Growth and Bone Metastasis

 

Chondrocyte-specific Knockout of Cbfβ Reveals the Indispensable Function of Cbfβ in Chondrocyte Maturation, Growth Plate Development and Trabecular Bone Formation in Mice

 

Ga13 negatively controls osteoclastogenesis through inhibition of the Akt-GSK3b-NFATc1 signalling pathway (See graphic at the bottom of the page)

 

Core binding factor beta (Cbfβ) controls the balance of chondrocyte proliferation and differentiation by up-regulating Indian hedgehog (Ihh) expression and inhibiting parathyroid hormone-related protein Receptor (PPR) expression in postnatal cartilage and bone formation

 

C/ebpα controls osteoclast terminal differentiation, activation, function, and postnatal bone homeostasis through direct regulation of Nfatc1

 

Monocyte-specific knockout of C/ebpα results in osteopetrosis phenotype, blocks bone loss in ovariectomized mice and reveals an important function of C/ebpα in osteoclast differentiation and function.

 

V-ATPase subunit ATP6AP1 (Ac45) regulates osteoclast differentiation, extracellular acidification, lysosomal trafficking, and protease exocytosis in osteoclast-mediated bone resorption

 

Specificity of RGS10A as a key component in the RANKL signaling mechanism for osteoclast differentiation

 

Deletion of Core-binding factor β (Cbfβ) in mesenchymal progenitor cells provides new insights into Cbfβ/Runxs complex function in cartilage and bone development

 

Ac45 silencing mediated by AAV-sh-Ac45-RNAi prevents both bone loss and inflammation caused by periodontitis

 

Cbfβ deletion in mice recapitulates cleidocranial dysplasia and reveals multiple functions of Cbfβ required for skeletal development

 

RNAi-Mediated Silencing of Atp6i and Atp6i Haploinsufficiency Prevents Both Bone Loss and Inflammation in a Mouse Model of Periodontal Disease

 

CCAAT/Enhancer-binding Protein (C/EBP) Is Important for Osteoclast Differentiation and Activity

 

Requirement of the Epithelium-specific Ets Transcription Factor Spdef for Mucous Gland Cell Function in the Gastric Antrum

 

RNA Interference-Mediated Silencing of Atp6i Prevents Both Periapical Bone Erosion and Inflammation in the Mouse Model of Endodontic Disease

 

Osteoclasts

We study osteoclast gene differentiation, function, positive and negative regulation, and signaling pathways.

Osteoclasts We study osteoclast gene differentiation, function, positive and negative regulation, and signaling pathways.