User:Mxt15/Evaluate an Article

Which article are you evaluating?
MTORC1

Why you have chosen this article to evaluate?
(Briefly explain why you chose it, why it matters, and what your preliminary impression of it was.)

I chose mTORC1 because of its relevance to my research and its role in transcription. mTORC1 is one of two complexes in the mTOR pathway. This specific complex has direct roles with downstream proteins needed for transcription such as S6 and euk. initiation factors. I found the article to give a good foundational layer of information about the complex and useful if someone wanted a brief understanding of mTORC1.

Evaluate the article
(Compose a detailed evaluation of the article here, considering each of the key aspects listed above. Consider the guiding questions, and check out the examples of what a useful Wikipedia article evaluation looks like.)

The mTORC1 article was well written and a great source of information for someone who wants a basic understanding of the function, pathways, and medical relevance of mammalian target of rapamycin complex 1. I don’t have too many concerns regarding the article, but there are two suggestions that I have to enhance the rigor and quality of the article.

·      The article devotes a section to upstream signaling of mTORC1. Specifically they discuss the Akt/PKB pathway, MAPK/ERK pathway, and the Wnt pathway. What more recent literature has shown is the JNK pathway directly activates mTORC1 via phosphorylation of RAPTOR.

·      I would also add more figures and images to enhance the article. The mammalian target of rapamycin complex 1 consists of various proteins. I think it would be beneficial for readers to see a cartoon figure representation of the substrates and proteins associated with the complex. Another figure I would add is a more detailed image of the pathways associated with mTORC1. The general upstream mTORC1 pathway is pretty useful and helpful to understanding the activation of mTORC1, but the downstream pathway could use some more details relating to how it effects transcription.

As a scientific article, the contributing authors do a well job in staying neutral and presenting the facts associated mTORC1. In looking at the references cited at the end of the article, a lot of the papers are older. While this doesn’t hinder the validity of the information presented, it does show that the article may be lacking current and new research that has added to our understanding of mTORC1.

The mTORC1 article was well written and a great source of information for someone who wants a basic understanding of the function, pathways, and medical relevance of mammalian target of rapamycin complex 1. I don’t have too many concerns regarding the article, but there are two suggestions that I have to enhance the rigor and quality of the article.

·      The article devotes a section to upstream signaling of mTORC1. Specifically they discuss the Akt/PKB pathway, MAPK/ERK pathway, and the Wnt pathway. What more recent literature has shown is the JNK pathway directly activates mTORC1 via phosphorylation of RAPTOR.

·      I would also add more figures and images to enhance the article. The mammalian target of rapamycin complex 1 consists of various proteins. I think it would be beneficial for readers to see a cartoon figure representation of the substrates and proteins associated with the complex. Another figure I would add is a more detailed image of the pathways associated with mTORC1. The general upstream mTORC1 pathway is pretty useful and helpful to understanding the activation of mTORC1, but the downstream pathway could use some more details relating to how it effects transcription.

As a scientific article, the contributing authors do a well job in staying neutral and presenting the facts associated mTORC1. In looking at the references cited at the end of the article, a lot of the papers are older. While this doesn’t hinder the validity of the information presented, it does show that the article may be lacking current and new research that has added to our understanding of mTORC1.