Talk:Transforming growth factor beta

Wiki Education Foundation-supported course assignment
This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Immcarle23. Peer reviewers: Immcarle22.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 11:38, 17 January 2022 (UTC)

Family of isoforms
First line says "...(TGF-β) is a protein that controls ...". Would it be more accurate and clearer to say "... (TGF-β) is a family of proteins that controls ..." since we have a separate article on TGF-β1 ? - Rod57 (talk) 14:41, 3 May 2011 (UTC)

or is the article about the single? mature TGF-β rather than the family of [isoforms of the] TGF-β precursors ? - Rod57 (talk) 15:16, 3 May 2011 (UTC)

Reliable review articles on TGF-beta function
The following is a list of review articles on the various elucidated functions of TGF-beta and its mechanisms of action. Any feedback or other directions of research that would help me improve this article would be appreciated!

Biancheri, P., Giuffrida, P., Docena, G., MacDonald, T., Corazza, G., and Di Sabatino, A. (2014). The role of transforming growth factor (TGF)-β in modulating the immune response and fibrogenesis in the gut. Cytokine Growth Factor Rev. 25, 45-55.

Massagué, J., and Xi, Q. (2012). TGF-β control of stem cell differentiation genes. FEBS Letters 586, 1953-1958.

Massagué, J., Blain, S., and Lo, R. (2000). TGF-b Signaling in Growth Control, Cancer, and Heritable Disorders. Cell 103, 295-309.

Massagué, J. (1998). TGF-β SIGNAL TRANSDUCTION. Annu. Rev. Biochem. 67, 753-791.

Massagué, J. (2008). TGF-β in Cancer. Cell 134, 215-230.

Seeger, P., Musso, T., and Sozzani, S. (2015). The TGF-β superfamily in dendritic cell biology. Cytokine Growth Factor Rev. 26, 647-657.

Shi, Y., and Massague, J. (2003). Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus. Cell 113, 685-700.

Immcarle23 (talk) 19:01, 31 January 2016 (UTC)

New and improved lead section
I find the current lead section for this article a little difficult to read due to its disorganization. Particularly, sentences like "TGF-beta is a secreted protein that controls [...] other functions in most cells" are too vague. Although I understand that not all of the functions of TGF-beta are known, I want to focus on the functions of TGF-beta for which there is substantial primary evidence. In particular, I am interested in expanding this article's coverage of TGF-beta's regulatory functions and role in the developing immune system. I also do not think that it is necessary to list all of the different diseases that TGF-beta may or may not play a role in or the specifics of its activation in the lead section. Instead, I want to focus on the outline of the article: TGF-beta's structure/activation and different functions, with perhaps a different sections for each function. Many of the existing sections can be combined. It is tempting to want to list all of the diseases that TGF-beta might play a role in, but such a discussion would be more useful in the context of TGF-beta's functions.

Draft new lead section: Transforming growth factor beta (TGF-β) is a pleiotropic cytokine belonging to the TGF-beta superfamily that includes three different isoforms (TGF-beta 1-3) and many other signaling proteins produced by all white blood cell lineages. Activated TGF-beta complexes with other factors to form a serine/threonine kinase that activates a signaling cascade that leads to the transcription of its many target genes, functioning in differentiation, chemotaxis, proliferation, and activation of many immune cells.

Among its key functions is regulation of inflammatory processes, particularly in the gut. TGF-beta also plays a crucial role in stem cell differentiation as well as T-cell regulation and differentiation. As such, it is a highly researched cytokine in the fields of cancer, auto-immune diseases, and infectious disease.

The TGF-beta superfamily includes endogenous growth inhibiting proteins; an increase in expression of TGF-beta oftens correlates with the malignancy of many cancers and a defect in the cellular growth inhibition response to TGF-beta. Its immuno-suppressive functions then come to dominate, contributing to oncogenesis. The disregulation of its immunosuppressive functions is also implicated in the pathogenesis of autoimmune diseases, although their effect is mediated by the environment of other cytokines present.

Existing lead section: ==== Transforming growth factor beta (TGF-β) is a secreted protein that controls proliferation, cellular differentiation, and other functions in most cells. It is a type of cytokine which plays a role in immunity, cancer, bronchial asthma, lung fibrosis, heart disease, diabetes, Hereditary hemorrhagic telangiectasia, Marfan syndrome, Vascular Ehlers-Danlos syndrome,[1] Loeys–Dietz syndrome, Parkinson's disease, Chronic kidney disease,[2] Multiple Sclerosis and AIDS. TGF-β is secreted by many cell types, including macrophages, in a latent form in which it is complexed with two other polypeptides, latent TGF-beta binding protein (LTBP) and latency-associated peptide (LAP). Serum proteinases such as plasmin catalyze the release of active TGF-β from the complex. This often occurs on the surface of macrophages where the latent TGF-β complex is bound to CD36 via its ligand, thrombospondin-1 (TSP-1). Inflammatory stimuli that activate macrophages enhance the release of active TGF-β by promoting the activation of plasmin. Macrophages can also endocytose IgG-bound latent TGF-β complexes that are secreted by plasma cells and then release active TGF-β into the extracellular fluid.[3] TGF-β exists in at least three isoforms called TGF-β1, TGF-β2 and TGF-β3. Until the three isoforms were discovered, TGF-β referred to TGF-β1, as it was the first member of this family to be discovered. The TGF-β family is part of a superfamily of proteins known as the transforming growth factor beta superfamily, which includes inhibins, activin, anti-müllerian hormone, bone morphogenetic protein, decapentaplegic and Vg-1. Most tissues have high expression of the genes encoding TGF-β. In contrast, other anti-inflammatory cytokines such as IL-10 show minimal expression in unstimulated tissues and seem to require triggering by commensal or pathogenic flora.[4] TGF-β acts as an antiproliferative factor in normal epithelial cells and at early stages of oncogenesis.[5] Some cells that secrete TGF-β also have receptors for TGF-β. This is known as autocrine signalling. Cancerous cells increase their production of TGF-β, which also acts on surrounding cells. ==== Immcarle23 (talk) 08:02, 10 February 2016 (UTC)

Suggested Edits
One of the things that I noticed was that you have a lot of subheadings. I would suggest that you could either combine some of these under a larger category or maybe even get rid of some of them. The Loeys–Dietz syndrome subheading for example just has one sentence and doesn't really contribute much to the arc of the page. I would also consider adding more to some other other categories such as heart disease.

In terms of organization you could also change some things around. For example you have types of TGFb very late in the page whereas I feel that this section deserves to have an earlier spot mostly because the section itself is more fundamental to understanding the page than is something like clinical significance.

There are also a few sections that could do with some more citations. There are a few subheadings under the function section that don't have any citations at all, and may viewed as unreliable as a result. The SMAD pathway section for example has a lot of information but is not backed by any sort of sources.

The lead in section however I thought was very well done and provides a fairly comprehensive overview of your article while preparing readers for what types of information to expect. My main critique right now is that there is a ton of information that would benefit greatly from some organization and re-structuring.

Great Job! Immcarle22 (talk) 22:15, 27 February 2016 (UTC)