Disease relevance of TGF1

• We observed two unusual patterns of cysteine and glycine residues in transforming growth factor type 1 (TGF1); our computer search found only one other protein, the 19-kilodalton early protein of vaccinia virus, having both patterns [1].
• Transforming growth factor-beta-induced growth inhibition and cellular hypertrophy in cultured vascular smooth muscle cells [2].
• Transforming growth factor (TGF)-beta(1)-mediated activation of tubular epithelial cells (TECs) is speculated to be a key contributor to the progression of tubulointerstitial fibrosis [3].
• Transforming growth factor-beta enhances adhesion of melanoma cells to the endothelium in vitro [4].
• Transforming growth factor (TGF)-beta is a potent inflammatory mediator involved in acute lung injury [5].

High impact information on TGF1

• Transforming growth factor-beta 1 is decreased in remodeling hypertensive bovine pulmonary arteries [6].
• Transforming growth factor-beta 1 modulates basic fibroblast growth factor-induced proteolytic and angiogenic properties of endothelial cells in vitro [7].
• Transforming growth factor beta, as well as plasmin inhibitors and anti-tissue type plasminogen activator antibody inhibited BCE cell invasion [8].
• Transforming growth factor-type beta (TGF-beta) has been identified as a constituent of bone matrix (Seyedin, S. M., A. Y. Thompson, H. Bentz, D. M. Rosen, J. M. McPherson, A. Conti, N. R. Siegel, G. R. Gallupi, and K. A. Piez, 1986, J. Biol. Chem. 261:5693-5695) [9].
• Transforming growth factor beta1 induction of vascular endothelial growth factor receptor 1: mechanism of pericyte-induced vascular survival in vivo [10].

Biological context of TGF1

• Transforming growth factor beta, at very low concentrations, suppressed the expression of the mineralization-related phenotype by chondrocytes [11].
• Transforming growth factor beta and fibroblast growth factor also restored cathodal-directed cell migration in serum-free medium [12].
• Transforming growth factor beta 1-mediated inhibition of smooth muscle cell proliferation is associated with a late G1 cell cycle arrest [13].
• In contrast, Transforming growth factor beta 1, which reduced slightly AT1 binding sites, but not the level of alpha q or alpha 11 proteins, did not change the A-II-induced inositol phosphate accumulation [14].
• Transforming growth factor (TGF)-beta 1 may have different effects on cell proliferation depending on many conditions [15].

Anatomical context of TGF1

• Transforming growth factor-beta 1 and forskolin modulate gap junctional communication and cellular phenotype of cultured Schwann cells [16].
• Transforming growth factor-beta induced gene-h3 (betaig-h3) was found to co-purify with collagen VI microfibrils, extracted from developing fetal ligament, after equilibrium density gradient centrifugation under both nondenaturing and denaturing conditions [17].
• Transforming growth factor beta1 decreases cholesterol supply to mitochondria via repression of steroidogenic acute regulatory protein expression [18].
• Transforming growth factor-alpha expression in the anterior pituitary gland: regulation by epidermal growth factor and phorbol ester in dispersed cells [19].
• Transforming growth factor-beta blocks proliferation but not early mitogenic signaling events in T-lymphocytes [20].

Associations of TGF1 with chemical compounds

• Transforming growth factor-beta 1 inhibits aldosterone biosynthesis in cultured bovine zona glomerulosa cells [21].
• Transforming growth factor beta 1 is a negative regulator of steroid 17 alpha-hydroxylase expression in bovine adrenocortical cells [22].
• Transforming growth factor beta 1 and adrenocorticotropin differentially regulate the synthesis of adrenocortical cell heparan sulfate proteoglycans and their binding of basic fibroblast growth factor [23].
• Transforming growth factor-beta 1 and ascorbate regulate proliferation of cultured smooth muscle cells by independent mechanisms [24].
• Transforming growth factor-beta stimulates retinoic acid-induced proteoglycan depletion in intact articular cartilage [25].

Regulatory relationships of TGF1

• Transforming growth factor beta1 regulates follistatin mRNA expression during in vitro bovine granulosa cell differentiation [26].
• Transforming growth factor-beta 1 inhibits aldosterone and stimulates adrenal renin in cultured bovine zona glomerulosa cells [27].
• Transforming growth factor alpha was found to stimulate the growth of normal bovine OSE and stroma cells to the same level as epidermal growth factor [28].

Other interactions of TGF1

• Transforming growth factor-beta and insulin-like growth factor-1 restore proteoglycan metabolism of bovine articular cartilage after depletion by retinoic acid [29].
• Transforming growth factor (TGF)-alpha, TGF-beta1, and TGF-beta2 are cytokines that regulate mammary gland development [30].
• Transforming growth factor beta1 blocks the release of collagen fragments from boving nasal cartilage stimulated by oncostatin M in combination with IL-1alpha [31].
• Transforming growth factor-alpha: identification in bovine corpus luteum by immunohistochemistry and northern blot analysis [32].

Analytical, diagnostic and therapeutic context of TGF1

• Transforming growth factor (TGF)-beta1 is associated with tumor progression and resistance to chemotherapy in established cancers, as well as host immune suppression [33].
• Transforming growth factor beta regulates the metabolism of proteoglycans in bovine cartilage organ cultures [34].

References