This article is rated Start-class on Wikipedia's content assessment scale. It is of interest to the following WikiProjects:

Molecular Biology: MCB / Cell Signaling This article is within the scope of WikiProject Molecular Biology, a collaborative effort to improve the coverage of Molecular Biology on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks.Molecular BiologyWikipedia:WikiProject Molecular BiologyTemplate:WikiProject Molecular BiologyMolecular Biology ??? This article has not yet received a rating on the importance scale. This article is supported by the Molecular and Cell Biology task force (assessed as Low-importance). This article is within the scope of the Cell Signaling task force, a task force which is currently considered to be inactive.

I saw that the stuff about EGF being used to treat diabetic foot ulcers was removed, citing Wikipedia:SOAP. I was the one that added that stuff and I don't have anything to do with those companies. If the problem with the content was that it was focusing on the companies too much then perhaps the info could still be kept but without referencing the companies. If the info just wasn't notable enough for inclusion then I guess that's fine too though. I thought that possible uses for the protein were interesting and relevant, but that's just me. Any other thoughts? Nanobri (talk) 05:09, 11 April 2008 (UTC)[reply]

"EGF results in cellular proliferation, differentiation, and survival. [1] This, in turn, results in an increased risk of cancer. [1]"

I believe this sentence and the opening paragraph does not stress the fact that EGF is a natural growth factor and only causes cancer when it's expression is up regulated. (AlexR)

That image is definitely not epidermal growth factor (EGF), but the EGF receptor, EGF is made up of 6 beta sheets and is a single monomer, certainly not two monomers.

I'm trying to change the image, but I'm a wikipedia newbie so taking my time.

OK seems I'm not allowed to, if anyone feels up to it, an appropriate image can be found at http://www.rcsb.org/pdb/explore.do?structureId=1A3P Mountainpenguin (talk) 00:46, 24 April 2009 (UTC)[reply]

The PDB: 1ivo​ structure that was displayed was of a complex of EGF and EGFR. I agree that this was somewhat confusing especially considering EGFR portion of the structure is much larger than the EGF portion. Per your request, I have replaced the 1ivo​ structure with 1a3p​. Cheers. Boghog2 (talk) 05:54, 24 April 2009 (UTC)[reply]

Could the Function section also mention what function, if any, it has in urine, milk and plasma ? eg do plasma levels vary to provide a signalling role ? In urine is it to help repair urinary tract tissues ? In milk is it for mother or childs benefit ? - Rod57 (talk) 10:07, 30 October 2016 (UTC)[reply]

Could we say something about the cell types that make it, the gene/genetics/epigenetics involved, and what factors (apart from testosterone) that affect the level and timing of production ? How does the EGF exit the cells that make it ? - Rod57 (talk) 10:16, 30 October 2016 (UTC)[reply]

Several news sources state that EGF is extracted from the foreskins of babies, maybe this should be addressed, especially if true. — Preceding unsigned comment added by 188.194.173.74 (talk) 11:33, 10 May 2018 (UTC)[reply]

In situ neutrophil efferocytosis shapes T cell immunity to influenza infection

Early recruitment of neutrophils from the blood to sites of tissue infection is a hallmark of innate immune responses. However, little is known about the mechanisms by which apoptotic neutrophils are cleared in infected tissues during resolution and the immunological consequences of in situ efferocytosis. Using intravital multiphoton microscopy, we show previously unrecognized motility patterns of interactions between neutrophils and tissue-resident phagocytes within the influenza-infected mouse airway. Newly infiltrated inflammatory monocytes become a chief pool of phagocytes and play a key role in the clearance of highly motile apoptotic neutrophils during the resolution phase. Apoptotic neutrophils further release epidermal growth factor and promote the differentiation of monocytes into tissue-resident antigen-presenting cells for activation of antiviral T cell effector functions. Collectively, these results suggest that the presence of in situ neutrophil resolution at the infected tissue is critical for optimal CD8+ T cell–mediated immune protection.

Cite: Lim, K., Kim, T., Trzeciak, A. et al. In situ neutrophil efferocytosis shapes T cell immunity to influenza infection. Nat Immunol 21, 1046–1057 (2020). https://doi.org/10.1038/s41590-020-0746-x

2.99.116.246 (talk) 12:06, 7 October 2020 (UTC)[reply]

Is the table under section Epidermal growth factor#Polypeptide growth factors necessary? kupirijo (talk) 16:11, 17 August 2022 (UTC)[reply]

Not only is Recombinant Human Epidermal Growth Factor (rhEGF) useful for diabetic foot ulcers, it is useful in aesthetic medicine, treating dermatoporosis (used to be called senile purpura/actinic purpura), hyperpigmentation, radiation skin injuries, atopic dermatitis, and in mitigating scars - via intradermal injection and topical applications.

• 'Epidermal Growth Factor in Aesthetics and Regenerative Medicine: Systematic Review'.

Miller-Kobisher, Suárez-Vega, Velazco de Maldonado. Journal of Cutaneous and Aesthetic Surgery. 2021 Apr-Jun;14(2):137-146.
Quote: "Similarities exist between the aging skin and wound healing, and mostly they involve the same oxidation and repair mechanisms..."

• 'The use of epidermal growth factor in dermatological practice'[literature review]

Sun Hye Shin, Young Gue Koh, Woo Geon Lee, Joon Seok, Kui Young Park. International Wound Journal. 2023 Aug;20(6):2414-2423.
Quote: "The extant literature demonstrates the therapeutic potential of rhEGF in dermatological conditions including various wounds, acne, radiation‐induced dermatitis, skin aging, and laser‐induced hyperpigmentation."

Thank you for your time, 2603:7000:D202:6D25:E15D:C5D7:5186:A3F2 (talk) 03:10, 30 July 2023 (UTC)[reply]