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Faculty Detail    
Name AMJAD JAVED
 
Campus Address SDB 714 Zip 0007
Phone 205-996-5124
E-mail javeda@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Oral & Maxillofacial Surgery  Oral & Maxillofacial Surgery Professor
Secondary  Biomedical Engineering  Biomedical Engineering Assistant Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Pathology   Pathology Chair Office Assistant Professor
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Biomedical Engineering  Biomatrix Eng Regen Med (BERM) Ctr Professor
Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  Comprehensive Ctr for Healthy Aging  Comprehensive Ctr for Healthy Aging Professor
Center  Medicine  Comprehensive Diabetes Ctr (Org Ret) Professor
Center  Cell, Developmntl, & Integrative Biology  Ctr for Exercise Medicine Professor
Center  Nutrition Sciences   Nutrition Obesity Res Ctr (NORC) Professor

Graduate Biomedical Sciences Affiliations
Cancer Biology 
Cell, Molecular, & Developmental Biology 
Cellular and Molecular Biology Program 
Genetics and Genomic Sciences 
Medical Scientist Training Program 

Biographical Sketch 
coming soon

Society Memberships
Organization Name Position Held Org Link
American Dental Education Association  Member  www.adea.org 
American Society for Bone and Mineral Research  Member  www.asbmr.org 
International Association for Dental Research  Member  www.iadr.com 

Research/Clinical Interest
Title
Genetic and Molecular Signaling for Cellular Differentiation and Skeletogenesis
Description
The central focus of our laboratory is to understand the molecular mechanisms that govern the formation and remodeling of skeletal tissues such as Cartilage, Bone, Teeth and Tendon. Cellular differentiation involves the stepwise establishment of specific genetic programs in proliferating cell lineages. We are exploring the signalling role of runt related transcription factor (Runx), in the coordinated regulation of various cell types (Chondrocyte, Osteoblast, Odontoblast) during skeletogenesis. Runx factors are heterodimers formed by α and β subunit and are essential for embryonic development. In mammals three genes encode α subunits (Runx1, 2 and 3) that recognize the same DNA sequences in target gene promoters yet exhibit distinct and non-redundant biological functions. Runx1 is required for definitive hematopoiesis and is frequently mutated in human leukemia. Runx2 is required for osteogenesis and in human mutations of the Runx2 gene are associated with cleidocranial dysplasia, an autosomal dominant skeletal disorder characterized by clavicular and pelvic anomalies, multiple supernumerary teeth, and a sever delay in closure of the fontanels. Runx3 controls neurogenesis, development and proliferation of the gastric epithelium and is frequently silenced in human gastric cancer. Runx2 knock-in and knock-out mouse models are lethal and show a complete absence of both intramembranous and endochondral ossification. Our lab utilizes conditional null model with biochemical, cellular, genetic and molecular approaches to identify molecular pathways during post-natal bone formation, bone remodeling, fracture healing, osteoporosis, osteoarthritis metabolic diseases (diabetes, obesity) and aging.

Selected Publications 
Publication PUBMEDID
Runx2 regulates gene network associated with insulin signaling and energy homeostasis. Cells Tissues Organs. 2011 May;194(2-4):232-237  21597275 
Chondrocyte specific regulatory activity of Runx2 is essential for survival and skeletal development. Cells Tissues Organs. 2011 May;194(2-4):161-165  21597273 
Genetic and transcriptional control of bone formation. Oral Maxillofac Surg Clin North Am. 2010 Aug;22(3):283-293.   20713262 
A Runx2 threshold for the cleidocranial dysplasia phenotype. Hum Mol Genet. 2009 Feb 1;18(3):556-68  19028669 
Oxidative stress induces vascular calcification through modulation of the osteogenic transcription factor Runx-2 by AKT signaling. J. Biol. Chem. 2008. May 30;283(22):15319-15327  18378684 
Structural coupling of Smad and Runx2 for execution of the BMP2 osteogenic signal. J. Biol. Chem. 2008 March 28 283(13): 8412-8422  18204048 
Mitotic occupancy and lineage-specific transcriptional control of rRNA genes by Runx2.
Nature. 2007 Jan 25;445(7126):442-6.
 
17251981 
Reconstitution of Runx2/Cbfa1-null cells identifies a requirement for BMP2 signaling through a Runx2 functional domain during osteoblast differentiation.
J Cell Biochem. 2007 Feb 1;100(2):434-49.
 
16927309  
Impaired intranuclear trafficking of Runx2 (AML3/CBFA1) transcription factors in breast cancer cells inhibits osteolysis in vivo.
Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1454-9. 
15665096  
Analysis of in vivo gene expression using epitope-tagged proteins.
Methods Mol Biol. 2004;285:37-40. 
15269395  
Cbfbeta interacts with Runx2 and has a critical role in bone development.
Nat Genet. 2002 Dec;32(4):639-44. 
12434156  
CCAAT/enhancer-binding proteins (C/EBP) beta and delta activate osteocalcin gene transcription and synergize with Runx2 at the C/EBP element to regulate bone-specific expression.
J Biol Chem. 2002 Jan 11;277(2):1316-23. 
11668178 
Subnuclear targeting of Runx/Cbfa/AML factors is essential for tissue-specific differentiation during embryonic development.
Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8650-5. 
11438701 
runt homology domain transcription factors (Runx, Cbfa, and AML) mediate repression of the bone sialoprotein promoter: evidence for promoter context-dependent activity of Cbfa proteins.
Mol Cell Biol. 2001 Apr;21(8):2891-905.
 
11283267  
Multiple Cbfa/AML sites in the rat osteocalcin promoter are required for basal and vitamin D-responsive transcription and contribute to chromatin organization.
Mol Cell Biol. 1999 Nov;19(11):7491-500.
 
10523637 

Keywords
Osteoblast, Bone Development, Gene Regulation, Osteoporosis