Amjad Javed
University of Alabama at Birmingham, AL·Biology
Building a skeleton requires cells to become bone-forming cells, called osteoblasts, at the right time and place. Two master switch proteins, Runx2 and Sp7, are both essential for this process.
- Fields
Biology
Genetics
Biochemistry
- Topics
Runx2
Sp7
osterix
- Grants
- 1 known grant, through Dec 2026
What they work on
- Measure natural Runx2 protein levels and stability in skeletal tissues of mice lacking Sp7, a bone-specific transcription factor, to test whether Sp7 is needed to keep Runx2 protein stable.
- Restore Sp7 selectively in bone precursor cells of Sp7-deficient mice to test whether this recovers Runx2 function and osteoblast formation.
- Map when and where Runx2–Sp7 regulatory complexes assemble during the formation and maintenance of osteoblasts, the bone-building cells.
- Define how posttranslational modifications, chemical tags on proteins, support stable Runx2–Sp7 complex formation and their ability to switch on skeletal genes.
More about the research
Without either one, bones fail to form. In people, mutations in Runx2 cause cleidocranial dysplasia, an inherited skeletal disorder. Mutations in Sp7 cause a recessive form of osteogenesis imperfecta, which leads to fragile bones. Why do these two seemingly unrelated proteins produce such similar defects?
Why it matters
Understanding how Runx2 and Sp7 work together to make bone cells mature could reveal parts of a bone-control complex that could be targeted by future therapies. Such therapies could improve cartilage and bone formation and repair. The work may also clarify the causes of growth disorders and metabolic bone diseases such as cleidocranial dysplasia and osteogenesis imperfecta.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Anne Delany
University of Connecticut, CT·Physiology
Characterize the bone structure and bone formation of male and female mice whose osteoblasts express a miR-433 'tough decoy' inhibitor, comparing mature and aging animals.
Sarah Dallas
University of Missouri-Kansas City, MO·Physiology
Determine how osteoblast movement, differentiation and fate are tied to collagen assembly and mineralization, using live-cell and intravital imaging of mice with GFP-tagged type I collagen and bone-lineage fluorescent reporters.
Fernando Fierro
University of California-Davis, CA·Physiology
Uncover how spermine synthase (SMS) deficiency impairs bone mineralization, testing whether excess spermidine blocks hypusination, the chemical activation of the protein eIF5A, and disrupts mitochondrial release of calcium phosphate.
The school
University of Alabama at Birmingham: 45 labs on PI Pages, $866M a year on research, 166 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.