TGFbeta

TGFβ

Farlex Partner Medical Dictionary © Farlex 2012

TGFB1

A gene on chromosome 19q13.1 that encodes a member of the transforming growth factor beta (TGFB) family of cytokines. These multifunctional peptides up- and downregulate proliferation, differentiation, adhesion, migration, death and other functions in many cell types. Active TGFB1 is either homodimeric or heterodimeric with other TGFB family members.

Molecular pathology
TGFB1 mutations cause Camurati-Engelmann disease; TGFB1 is often upregulated in tumour cells.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.
References in periodicals archive ?
Bakay et al., "Early onset of inflammation and later involvement of TGFbeta in Duchenne muscular dystrophy," Neurology, vol.
Asiaticoside induces human collagen I synthesis through TGFbeta receptor I kinase (TbetaRI kinase)-independent Smad signaling.
Cartilage chondrocytes are known to be extremely long lived and undergo changes with age, which result in modifications in their anabolic and catabolic processes and include a reduced responsiveness to growth factors, such as TGFbeta, BMPs, and WNT [54].
Alvares, and P Gama, "Ontogenic expression of TGFbeta 1, 2, and 3 and its receptors in the rat gastric mucosa," Developmental Dynamics, vol.
Oswald et al., "TGFbeta receptor mutations impose a strong predisposition for human allergic disease," Science Translational Medicine, vol.
Hinck, Shu Z et al., "Three key residues underlie the differential affinity of the TGFbeta isoforms for the TGFbeta type II receptor," Journal of Molecular Biology, vol.
Wang et al., "Inhibition of autoregulated TGFbeta signaling simultaneously enhances proliferation and differentiation of kidney epithelium and promotes repair following renal ischemia," American Journal of Pathology, vol.
Krieglstein, "TGFbeta signalling plays an important role in IL4-induced alternative activation of microglia," Journal of Neuroinflammation, vol.
Paired t test measurement of repeated multiple analysis was performed to the level of Treg cells and TGFbeta between the two groups at the same phase, or during different phases of treatment and followup.
Liver disease was simulated in this unique experimental model by application of the potent, profibrotic molecules, TGFbeta and PDGF.
C/EBPbeta at the core of the TGFbeta cytostatic response and its evasion in metastatic breast cancer cells.