TGFB1 | SelfDecode | Genome Analysis

Summary of TGFB1

TGF-beta plays an important role in autoimmune diseases, food intolerances, cancer, cognitive function, wound healing and other diseases.

TGF-b is a cytokine that affects the growth and proliferation of many cell types, and it has pro- and anti-inflammatory effects. Summary of Activities of TGF-beta:

Causes collateral damage in infections
Causes the growth/changes in tissue
Decreased acetylcholine
Decreased slow wave or deep sleep
Decreases muscle regeneration
Decreases the action of the vitamin D receptor
Increases free radicals
Can decrease bone density
It inhibits proliferation of most other cell types
Suppresses red blood cell formation and lymphocytes (T and B cells)
Suppresses antibody production
Suppresses Cytotoxic T Cell (CD8) and Natural Killer cell activity...this can cause viral infections to get out of control.
Deactivates macrophages
Promotes oral tolerance
Suppresses inflammation
Promotes wound healing and new blood vessel formation (angiogenesis)
Induces local inflammation and fibrosis
Stimulates extracellular matrix deposition
Promotes switch to IgA
Can increase cancer growth
Cause negative changes in the airways
Can benefit cognitive function (when very mildly elevated)

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The Function of TGFB1

Multifunctional protein that controls proliferation, differentiation and other functions in many cell types. Many cells synthesize TGFB1 and have specific receptors for it. It positively and negatively regulates many other growth factors. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Can promote either T-helper 17 cells (Th17) or regulatory T-cells (Treg) lineage differentiation in a concentration-dependent manner. At high concentrations, leads to FOXP3-mediated suppression of RORC and down-regulation of IL-17 expression, favoring Treg cell development. At low concentrations in concert with IL-6 and IL-21, leads to expression of the IL-17 and IL-23 receptors, favoring differentiation to Th17 cells. Mediates SMAD2/3 activation by inducing its phosphorylation and subsequent translocation to the nucleus (PubMed:25893292). Can induce epithelial-to-mesenchymal transition (EMT) and cell migration in various cell types (PubMed:25893292).

Protein names

Recommended name:

Transforming growth factor beta-1

Short name:

LAP

Alternative name(s):

TGF-beta-1

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RS1800469 (TGFB1) ??
RS1800470 (TGFB1) ??
RS1800471 (TGFB1) ??
RS1800472 (TGFB1) ??
RS2241715 (TGFB1) ??
RS4803455 (TGFB1) ??
RS8110090 (TGFB1) ??

Top Gene-Substance Interactions

TGFB1 Interacts with These Diseases

Disease	Score

Fixes

TGF-beta Inhibitors

If you have genes that cause high TGF-beta, you might do better with TGF inhibitors. These inhibit TGF in different places, but not necessarily systemically....

Sun/UV (R, R2) - at least in skin cells.
Curcumin (R),
Black Cumin Seed Oil /Thymoquinone (R) -in rat model of allergic airway inflammation,
Andrographis/Andrographolide (R),
Extra Virgin Olive Oil (R),

Fixes Advanced

TGF increases ROS, but Butyrate helps prevent this. (R)

If you have systemically high TGF, you might want to take a mito antioxidant such as MitoQ, since much of the damage from TGF is by increasing ROS in your mitochondria. (R, R2)

Other TGF-beta Inhibitors

If you have genes that cause high TGF-beta, you might do better with TGF inhibitors. These inhibit TGF in different places, but not necessarily systemically....

PPAR agonists (gamma and alpha) (R, R2, R3, R4) - reduces TGF in blood vessels and the negative effects of TGF in skin, heart muscle and liver cells... PPAR gamma can be considered anti-TGF overall.
Vitamin D Receptor activation (R), Angiotensin II type 1 receptor antagonist (R)
Klotho - Specifically, Klotho was shown to bind to the TGF-²1 receptor to inhibit TGF-²1 binding (R).
Ursolic acid (R),
Reishi (R),
Fucoidan (R),
Resveratrol (R),
Apigenin (R),
Berberine (R),
Quercetin(R),
Grape Seed Extract (R),
Ginkgo (R),
Pregnenolone (R)
Astragalus (R, R2),
Zinc,
Silymarin/Silibinin,
Hesperidin,
Garlic,
Gotu Kola /Asiatic Acid,
Emodin (found in Fo-Ti, Resveratrol, Rhubarb, Aloe),
Theanine (R),
Naringenin,
Ginseng (R),
Kudzu root/Puerarin,
Angelica S, Hydrangea, Dan Shen, Almond, Cordyceps, Butein, Betulinic acid,
Enterococcus faecalis (R)****,

TGF-beta Increasers

You want to be careful about the following if you have genes that cause higher TGF-beta.

Hypoxia (R) or low oxygen
SIRT1 (R) - maybe resveratrol is not a great idea
Pregnenolone (R ), - increases Th2 dominance...
Estrogen (R) - increased TGF in skin
T3 (R)
Progesterone (R, R2) - increased TGF in epithelial cells...which are all over the body...
S Boulardii (R) - TGF increased in the blood in chicks.
Bacillus Subtilis (R) - TGF increased in the blood in chicks.
Artemisinin (R) - increased TGF in spleen cells,
AngiotensinII- increased TGF in heart (R),
Beta-2 Adrenoreceptor (R) agonism, increased TGF in the hippocampus...

Substances That Increase TGFB1

Category:

Substances	Interaction	Organism	Category

Substances That Decrease TGFB1

Category:

Substances	Interaction	Organism	Category

Advanced Summary

Read/FIX: TGF Beta: What It Does And Natural Ways to Inhibit and Increase It TGF-beta is produced in cells such as platelets, macrophages, B- and T-lymphocytes, fibroblasts, ECs, osteoblasts and osteoclasts, astrocytes, and microglial cells.

The thymus, bone marrow and bone also produce TGF . There are different types of TGF, but TGF-b1 is the main one involved in immunity.

TGF-beta is often very elevated in people with biotoxin/mold issues. Blood TGF is highly significantly correlated with the platelet count, probably because most of the TGF is released by platelets. (R) You want TGF to be balanced rather than too high or too low...

The Good (Sometimes)

TGF increases serotonin transporters and serotonin uptake in the gut, which is low in IBS and IBD. (R) So this suggests that TGF is protective against autoimmune gut disorders. TGF is increased by helminthic therapy and this is one important mechanism by which it's protective against colitis. (R)

Studies have shown that TGF-b in the gut area is necessary to create tolerance orally. (R)

The primary mechanisms of oral tolerance are the active suppression of immune responses through the induction of regulatory T cells in the gut-associated lymphoid tissue. These Th3 cells secrete TGF-b, IL-4, and IL-10, which decrease Th1 and other immune cells.

TGF-b also leads to the death of T cells that attack our tissue (clonal deletion). (R)

Due to its potent anti-proliferative effects, TGF-b normally functions as a tumor suppressor. However, cancer cells develop resistance to TGF-b late in tumor progression by using multiple mechanisms.

TGF-b promotes wound healing due to its unique effect on the extracellular matrix by stimulating the synthesis of matrix proteins and decreased matrix degradation.

In infections, it protects against collateral damages caused by the immune system, but it also promotes immune evasion by pathogens and therefore can lead to chronic infections.

TGF-b suppresses the immune system at the systemic level but stimulates the immune and inflammatory responses at the local level.

TGF-b1 deficient mice develop an inflammatory response with massive white blood cell infiltration in numerous organs, accompanied by increased expression of TNF-a, IFN-g, and class I and II MHC antigens, resulting in death at 3 to 5 weeks.

These mice also have high levels of autoantibodies. Thus, TGF-b1 normally acts as an active suppressor of inflammation. TGF-b can suppress the proliferation of T- and B-lymphocytes, monocytes, and macrophages.

It suppresses immunoglobulin (Ig) secretion of mature B cells, but can increase IgA production (not a cause of autoimmunity). TGF-b inhibits IFN-g, IL-2, IL-3, GM-CSF, and TNF-a in response to infections or other stimuli.

TGF-b also decreases E-selectin and IL-8 on blood vessels. TGF-b can deactivate macrophages by reducing their capacity to release superoxide and nitric oxide, suppressing their cytotoxic activity, decreasing their expression of MHC class II, inhibiting the production of TNF-a and IL-1, and antagonizing the effects of these cytokines.

TGF-b can also benefit cognitive function. One study found TGF-beta was associated with increased cortical thickness, and this is thought in part to do with the reduction of cytokines. (R) TGF is low in advanced atherosclerosis.

The Bad

TGF-b can increase inflammation locally. TGF-b inhibits acetylcholine formation (in muscle and spinal cells) (R). Inhibition of acetylcholine formation elegantly explains many of the symptoms that CIRS people have (R). In an inflammatory environment, it will produce proinflammatory Th17 and Th9 cells (instead of Tregs) and inhibit Th22 cells. (R)

TGF-b suppresses red blood cells by inhibiting bone marrow stem-cell proliferation and decreasing the expression of receptors for SCF400, IL-3, and GM-CSF in hematopoietic cells (R).

One thing that is interesting is that I have a client/friend with high TGF and low RBCs. This makes sense because TGF decreases RBC formation.

In cancer, TGF-² is a potent inhibitor of cell proliferation and acts as a tumor suppressor at the beginning of tumor formation. However, once the cells become resistant to TGF-², it mainly supports tumor growth and metastasis by promoting immune evasion and angiogenesis. (R)

TGFbeta decreases slow wave sleep (R, R2). TGF-b decreases muscle regeneration (R), which is one reason why people with CIRS lose muscle. TGF-b will increase VEGF , by increasing hypoxia inducible factor, which can make tumors spread. (R, R2)

Indeed, an elevated blood level of TGF-b significantly correlated with lymph node metastasis and poor prognosis in patients with gastric cancer. (R) TGF-beta decreases the action of the vitamin D receptor (R).

In asthma, TGF-b is assumed to promote allergen tolerance, but plays a detrimental role in irreversible tissue changes of the airways. (R)

TGF-b causes various cells to stick to the site of inflammation and tissue injury (chemotaxis). These include neutrophils, monocytes, lymphocytes, mast cells, and fibroblasts; TGF-beta also activates these cells to produce inflammatory cytokines (IL-1, TNF, and IL-6); and causes white blood cells to stick to the vessel wall and Extracellular matrix.

TGF-b secretion is increased by male hormone treatment in certain hair cells. Androgens increase ROS, which increases TGF . (R) TGF-b has both positive and negative effects on bone mineral density.

It's thought by scientists that in the short term in can help bone density, but chronically elevated TGF-b will decrease bone density. (R)

TGF-b has been proposed as a contributing factor in many chronic inflammatory diseases, which include rheumatoid arthritis, glomerulonephritis, pulmonary fibrosis, systemic sclerosis, and chronic hepatitis.

TGF-b is elevated in the blood of patients with invasive prostate cancer.

Camurati-Engelmann disease Approximately 10 mutations in the TGFB1 gene have been found to cause Camurati-Engelmann disease. Most of the mutations change one protein building block (amino acid) in the TGFβ-1 protein. The most common mutation replaces the amino acid arginine with the amino acid cysteine at position 218 in the TGFβ-1 protein (written as Arg218Cys or R218C). All mutations that cause Camurati-Engelmann disease result in a TGFβ-1 protein that is always turned on (active). The overactive protein likely disrupts the regulation of bone growth and impairs muscle and body fat development. A disruption in the regulation of TGFβ-1 activity can lead to increased bone density and other features of Camurati-Engelmann disease. cancers Some TGFB1 gene mutations are acquired during a person's lifetime and are present only in certain cells. These changes are called somatic mutations and are not inherited. Somatic mutations in the TGFB1 gene that cause alterations in the activity (expression) of the TGFβ-1 protein are associated with certain cancers. The altered protein expression may enhance several cancer-related events such as cell division (proliferation), cell motility, and the development of new blood vessels (angiogenesis) that nourish a growing tumor. The TGFβ-1 protein is abnormally active (overexpressed) in certain types of prostate cancers. Altered TGFβ-1 expression has also been found in breast, colon, lung, and bladder cancers. A variation (polymorphism) in the TGFB1 gene that changes a single amino acid in the TGFβ-1 protein is associated with prostate cancer. In people with this polymorphism, the amino acid leucine is replaced with the amino acid proline at position 10 in the TGFβ-1 protein. Although it has no apparent effect in healthy people or those with a condition caused by a different mutation in the TGFB1 gene, this polymorphism is associated with accelerated disease progression and a poorer outcome in patients with prostate cancer.

The TGFB1 gene provides instructions for producing a protein called transforming growth factor beta-1 (TGFβ-1). The TGFβ-1 protein helps control the growth and division (proliferation) of cells, the process by which cells mature to carry out specific functions (differentiation), cell movement (motility), and the self-destruction of cells (apoptosis). The TGFβ-1 protein is found throughout the body and plays a role in development before birth, the formation of blood vessels, the regulation of muscle tissue and body fat development, wound healing, and immune system function. TGFβ-1 is particularly abundant in tissues that make up the skeleton, where it helps regulate bone growth, and in the intricate lattice that forms in the spaces between cells (the extracellular matrix). Within cells, this protein is turned off (inactive) until it receives a chemical signal to become active.

Conditions with Increased Gene Activity

Experimental Variables:

Condition	Change (log₂fold)	Comparison	Species	Experimental variables	Experiment name

Conditions with Decreased Gene Activity

Experimental Variables:

Condition	Change (log₂fold)	Comparison	Species	Experimental variables	Experiment name

Technical

The following transcription factors affect gene expression:

Tissue specificity:

Highly expressed in bone. Abundantly expressed in articular cartilage and chondrocytes and is increased in osteoarthritis (OA). Colocalizes with ASPN in chondrocytes within OA lesions of articular cartilage.

Gene Pathways:

Induction:

Activated in vitro at pH below 3.5 and over 12.5.

Molecular Function:

Biological Processes:

Drug Bank:

Hyaluronidase
Hyaluronidase (Human Recombinant)

*synonyms

Synonyms/Aliases/Alternative Names of the Gene:

TGFB1 (Transforming growth factor beta 1)

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