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This arrests the cell cycle in G1 phase, inducing senescence without apoptosis. [10] Therefore, it is only effective in melanomas with a BRAF mutation, which make up 50% of all melanomas. [ 11 ] The plasma elimination half-life of encorafenib is approximately 6 hours, occurring mainly through metabolism via cytochrome P450 enzymes.
Plants can protect themselves from abiotic stress in many different ways, and most include a physical change in the plant’s morphology. Phenotypic plasticity is a plant’s ability to alter and adapt its morphology in response to the external environments to protect themselves against stress. [ 2 ]
BRAF is a human gene that encodes a protein called B-Raf. The gene is also referred to as proto-oncogene B-Raf and v-Raf murine sarcoma viral oncogene homolog B, while the protein is more formally known as serine/threonine-protein kinase B-Raf. [5] [6] The B-Raf protein is involved in sending signals inside cells which are involved in directing ...
The proteinase inhibitors work to disrupt the enzymatic ability of the digestive or microbial enzymes that are present in the stomach of the attacker resulting in the inability to properly digest the plant material. This causes an interference of proper growth and discourages further wounding of the plant by the attacker. [1]
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Systemin is a plant peptide hormone involved in the wound response in the family Solanaceae. It was the first plant hormone that was proven to be a peptide having been isolated from tomato leaves in 1991 by a group led by Clarence A. Ryan. Since then, other peptides with similar functions have been identified in tomato and outside of the ...
V600E is a mutation of the BRAF gene in which valine (V) is substituted by glutamic acid (E) at amino acid 600. [1] [2] It is a driver mutation in a proportion of certain diagnoses, including melanoma, [3] [4] hairy cell leukemia, [5] [6] papillary thyroid carcinoma, [7] [8] colorectal cancer, [9] non-small-cell lung cancer, [10] [11] Langerhans cell histiocytosis, [12] Erdheim–Chester ...
Vemurafenib causes programmed cell death in melanoma cell lines. [3] Vemurafenib interrupts the B-Raf/MEK step on the B-Raf/MEK/ERK pathway − if the B-Raf has the common V600E mutation. Vemurafenib only works in melanoma patients whose cancer has a V600E BRAF mutation (that is, at amino acid position number 600 on the B-Raf protein, the ...