The multifunctional nature of TGF-ß is underscored
by its involvement in a broad range of research fields. TGF-ß has been implicated
as a regulator of biological functions in cancer, development, endocrinology,
immunology, neuroscience, proteases, and stem cells. Please note that references
cited here are not judged for inclusion (or exclusion) based on scientific
merit. Rather, they are a random selection of
references on TGF-ß research from a broad range of fields that have been
published between January and March of 2005.
CANCER
- Dubrovska, A. et al. (2005) TGFb1/Smad3 counteracts BRCA1-dependent repair of DNA damage.
Oncogene [epub ahead of print Feb 14].
- Muraoka-Cook, R.S. et al. (2005) Dual role of transforming growth factor ß in
mammary tumorigenesis and metastatic progression. Clin. Cancer Res. 11:937s.
DEVELOPMENT
- Corday, P. & D.J. Satterwhite (2005) TGF-ß induces novel Lef-1 splice variants
through a Smad-independent signaling pathway. Dev. Dyn. [epub ahead of print
Feb 25].
- Loeys, B.L. et al. (2005) A syndrome of altered cardiovascular, craniofacial,
neurocognitive and skeletal development caused by mutations in TGFß R1 and
TGFß R2. Nat. Genet. 37:275.
ENDOCRINOLOGY
- Park, K.S. et al. (2005) Genetic polymorphisms in the transforming growth factor
beta-induced gene associated with BMI. Hum. Mutat. 25:322.
- Solini, A. et al. (2005) Purinergic modulation of mesangial extracellular matrix
production: role in diabetic and other glomerular diseases. Kidney Int. 67:875.
IMMUNOLOGY
- Chen, M.L. et al. (2005) Regulatory T cells suppress tumor-specific CD8 T cell
cytotoxicity through TGF-ß signals in vivo. Proc. Natl. Acad. Sci. USA 102:419.
- Scherf, W. et al. (2005) Reduced expression of transforming growth factor ß1 exacerbates
pathology in an experimental asthma model. Eur. J. Immunol. 35:198.
NEUROSCIENCE
- Lee, E.O. et al. (2005) The amyloid-ß peptide suppresses transforming growth
factor-ß1-induced matrix metalloproteinase production via Smad7 expression
in human monocyte THP-1 cells. J. Biol. Chem. 280:7845.
- Wurdak, H. et al. (2005) Inactivation of TGFß signaling in neural crest stem
cells leads to multiple defects reminiscent of DiGeorge syndrome. Genes Dev.
19:530.
PROTEASES
- Berg, D.T. et al. (2005) Smad6s regulates plasminogen activator inhibitor-1
through a PKC-beta dependent up-regulation of TGF-ß. J. Biol. Chem. [epub
ahead of print Feb 16].
- Kim, H.S. et al. (2005) Doxycycline inhibits TGF-ß1-induced MMP-9 via Smad
and MAPK pathways in human corneal epithelial cells. Invest. Ophthalmol. Vis.
Sci. 46:840.
STEM CELLS
- James, D. et al. (2005) TGFß/Activin/Nodal signaling is necessary for the maintenance
of pluripotency in human embryonic stem cells. Development [epub ahead of
print Feb 9].
- Wei, C.L. et al. (2005) Transcriptome profiling of human and murine ESCs identifies
divergent paths required to maintain the stem cell state. Stem Cells 23:166.
|