INT9130

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Context Info
Confidence 0.41
First Reported 1992
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 16
Total Number 17
Disease Relevance 12.21
Pain Relevance 2.92

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

aging (TGFB1) enzyme binding (TGFB1) embryo development (TGFB1)
cytoplasm (TGFB1) extracellular space (TGFB1) extracellular region (TGFB1)
Anatomy Link Frequency
plasma 1
smooth muscle 1
capillary 1
lung 1
nucleus pulposus 1
TGFB1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Multiple sclerosis 13 99.66 Very High Very High Very High
Inflammation 115 99.62 Very High Very High Very High
c fibre 5 99.24 Very High Very High Very High
fibrosis 96 99.02 Very High Very High Very High
cytokine 116 98.80 Very High Very High Very High
bradykinin 21 94.96 High High
sodium channel 18 89.56 High High
Pain 9 87.04 High High
antagonist 20 85.80 High High
Inflammatory response 7 83.84 Quite High
Disease Link Frequency Relevance Heat
Cancer 154 100.00 Very High Very High Very High
Necrosis 17 100.00 Very High Very High Very High
Camurati-engelmann Disease 12 100.00 Very High Very High Very High
Hypercalcemia 10 99.96 Very High Very High Very High
Demyelinating Disease 12 99.66 Very High Very High Very High
INFLAMMATION 156 99.62 Very High Very High Very High
Osteoporosis 14 99.36 Very High Very High Very High
Congenital Anomalies 16 99.20 Very High Very High Very High
Pulmonary Fibrosis 65 99.02 Very High Very High Very High
Metastasis 13 98.78 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
IFN-gamma and TGF-beta may have opposing effects in MS, and treatments inhibiting IFN-gamma and/or promoting TGF-beta might ameliorate MS.
Negative_regulation (inhibiting) of TGF-beta associated with multiple sclerosis
1) Confidence 0.41 Published 1994 Journal Ann. Neurol. Section Abstract Doc Link 8080246 Disease Relevance 1.05 Pain Relevance 0.61
As an example, up-regulation in NHEK after 24 hrs was seen for transcripts encoding CDKN2B (p15), which is believed to be an effector of TGF-?
Negative_regulation (effector) of TGF
2) Confidence 0.37 Published 2005 Journal BMC Cancer Section Body Doc Link PMC1182358 Disease Relevance 0.44 Pain Relevance 0.04
Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta.
Negative_regulation (diminished) of TGF-beta associated with osteoporosis
3) Confidence 0.30 Published 1998 Journal J. Cell. Biochem. Section Title Doc Link 9712146 Disease Relevance 0.85 Pain Relevance 0.09
One class encodes proteins known to contribute to osteogenic differentiation and/or inhibit hMSC growth (FHL2, POSTN, LOX, LOXL1, SPARC, TMSB4X, CTHR1, FST, TGFB1) while a second contains markers for a closely related differentiation fate of hMSC, chondrogenesis (CHI3LI, COL1A1, COL3A1, COL6A3, COL8A1, COL12A1, CTGF, LUM).
Negative_regulation (inhibit) of TGFB1
4) Confidence 0.23 Published 2008 Journal BMC Syst Biol Section Body Doc Link PMC2527292 Disease Relevance 0.13 Pain Relevance 0.03
When A- and C-fiber were activated at the same time, the C-CED might be inhibited by the A-fiber inputs.
Negative_regulation (inhibited) of C-CED associated with c fibre and camurati-engelmann disease
5) Confidence 0.22 Published 1992 Journal Brain Res. Section Abstract Doc Link 1393533 Disease Relevance 0.53 Pain Relevance 0.43
The inductive activity of TGF-beta1 on collagen deposition and the number of dermal cells immunoreactive for vimentin and alpha-smooth muscle actin was significantly suppressed by injection of alpha-MSH.
Negative_regulation (suppressed) of TGF-beta1 in smooth muscle
6) Confidence 0.18 Published 2004 Journal J. Biol. Chem. Section Abstract Doc Link 14645373 Disease Relevance 0.10 Pain Relevance 0.19
Further studies demonstrate that FGF2 (10 ng/ml) antagonizes BMP7-mediated acceleration of PG production in bovine nucleus pulposus cells via the upregulation of noggin, an inhibitor of the transforming growth factor beta/bone morphogenetic protein signaling pathway.
Negative_regulation (inhibitor) of transforming growth factor beta in nucleus pulposus
7) Confidence 0.16 Published 2008 Journal Arthritis Res Ther Section Abstract Doc Link PMC2453768 Disease Relevance 0.05 Pain Relevance 0.04
After bleomycin instillation, osteopontin-null mice developed reduced lung fibrosis characterized by dilated distal air spaces with decreased active transforming growth factor-beta 1 (TGF-?
Negative_regulation (decreased) of transforming growth factor-beta 1 in lung associated with fibrosis and pulmonary fibrosis
8) Confidence 0.10 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC1198037 Disease Relevance 1.04 Pain Relevance 0.40
Osteolytic metastases can be suppressed in vivo by inhibition of bone resorption, blockade of TGFbeta signaling in tumor cells, and by neutralization of PTHrP.
Negative_regulation (blockade) of TGFbeta associated with cancer, hypercalcemia and metastasis
9) Confidence 0.10 Published 2000 Journal Crit. Rev. Eukaryot. Gene Expr. Section Abstract Doc Link 11186331 Disease Relevance 1.71 Pain Relevance 0
Retinoic acid has been demonstrated to be a key regulator of TGF-beta dependent immune responses, capable of inhibiting the IL-6-driven induction of proinflammatory TH17 cells and promoting anti-inflammatory Treg cell differentiation [70].

7.

Negative_regulation (regulator) of TGF-beta associated with inflammation
10) Confidence 0.06 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2821644 Disease Relevance 0.32 Pain Relevance 0.13
This effect was reversible by removal of transforming growth factor beta 1 (TGF-beta 1) from the culture medium and could be reproduced by the addition of TGF-beta 1 to normal nasal mucosa [9].


Negative_regulation (removal) of transforming growth factor beta 1 in nasal mucosa
11) Confidence 0.06 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.82 Pain Relevance 0.14
Supporting the importance of the ALK5 receptor, pharmacologically inhibiting ALK5 signaling with the potent inhibitor SB431542 [74], [75] prevented TGF?
Negative_regulation (prevented) of TGF
12) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2832687 Disease Relevance 0.09 Pain Relevance 0.04
TGF beta1 was found to lead to perinuclear accumulation of CFTR protein and reduced chloride secretory responses to cAMP stimulating agents [82].
Negative_regulation (reduced) of TGF beta1
13) Confidence 0.05 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.33 Pain Relevance 0.24
VEGFR Tyrosine Kinase Inhibitors

Cediranib (AZD2171, CED) is a highly selective and potent oral tyrosine kinase inhibitor (TKI) of VEGFR1, VEGFR2, VEGFR3, and c-Kit.

Negative_regulation (inhibitor) of CED associated with camurati-engelmann disease
14) Confidence 0.04 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2804796 Disease Relevance 2.18 Pain Relevance 0.32
Pioglitazone also reduced inflammation, as manifested by reductions in C-reactive protein (CRP), tumor necrosis factor alpha, and transforming growth factor-beta, and increased plasma adiponectin levels.


Negative_regulation (reductions) of transforming growth factor-beta in plasma associated with necrosis, inflammation and cancer
15) Confidence 0.02 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2941781 Disease Relevance 1.36 Pain Relevance 0.18
Low dose GH was found to prevent the reduced capillary length density and increased fibroblast volume density, with reduced collagen and transforming growth factor-beta (TGF-beta); aortic abnormalities were not affected.
Negative_regulation (reduced) of transforming growth factor-beta in capillary associated with congenital anomalies
16) Confidence 0.01 Published 2010 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC3024648 Disease Relevance 1.12 Pain Relevance 0.07
CONCLUSION: The results suggest that deficiencies of IL-1ra, IL-10, and TGF-beta1 probably play an important role in the cause and pathogenesis of TMJ ID and OA.


Spec (probably) Negative_regulation (deficiencies) of TGF-beta1
17) Confidence 0.01 Published 1999 Journal J. Oral Maxillofac. Surg. Section Body Doc Link 10437719 Disease Relevance 0.06 Pain Relevance 0

General Comments

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