| Autor: |
Antony Reneese, P. Joseph, Kasilingam, S., Ragavi, M., Boominathan, Meganathan, Muthukumar, Sivaramapillai, Razia, M., Ramaiyan, Sankar |
| Předmět: |
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| Zdroj: |
Journal of Experimental Zoology India; Jul2024, Vol. 27 Issue 2, p2257-2264, 8p |
| Abstrakt: |
The Kirsten rat sarcoma viral oncogene homolog, or KRAS gene is an oncogene that produces the small GTPase transductor protein known as KRAS. Because it may transmit outside signals to the cell nucleus, KRAS plays a role in controlling cell division. Mutations that activate the KRAS gene hinder the KRAS protein's capacity to transition between active and inactive states, which can cause cell transformation and heightened resistance to treatments that target epidermal growth factor receptors, such as chemotherapy and biological therapies. One of the leading causes of cancer-related death worldwide is colon adenocarcinoma. A mutation in KRAS causes your cells to proliferate uncontrollably, leading to the development of cancer. A wild-type gene is an ordinary (unmutated) gene. KRAS, an acronym for Kirsten rat sarcoma, is a gene that is altered in colorectal cancer quite commonly. Additionally connected to pancreatic and lung cancers are mutated forms of this gene. In this research work, we investigated the effect of Lactobacillus plantarum generated SCFA on the expression level of the KRAS gene. The level of KRAS gene expression was significantly lower, according to the data. With a rise in SCFA concentration, the fold change was lessened; at 100 µg/ml, the fold change value was less. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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