Explore chapters and articles related to this topic
Protease Involvement in Sperm Motility
Published in Claude Gagnon, Controls of Sperm Motility, 2020
Eve de Lamirande, Marie-Paule Cosson, Claude Gagnon
The molecular mechanisms for muscle contraction and axonemal movement have often been compared24 since they both include the involvement of transitory cross-bridges and a sliding process (actin-myosin and adjacent microtubules, respectively). Whether these cross-bridges are of covalent or ionic nature is still unknown. Even though the current theory favors an ionic interaction, a theory of covalent bonding between actin and myosin in muscle contraction, involving the formation (through a transglutaminase) and the splitting (through an isopeptidase) of cross-links, has been proposed in the past.25
A novel compound heterozygous mutation of MYSM1 gene in a patient with bone marrow failure syndrome 4
Published in British Journal of Biomedical Science, 2021
X Zhan, A Zhao, B Wu, Y Yang, L Wan, P Tan, J Huang, Y Lu
MYSM1 includes 3 domains: SANT, SWIRM and JAB. The SANT domain is present in nuclear receptor co-repressors and in the subunits of many chromatin-remodelling complexes [18]. It has a strong structural similarity to the DNA-binding domain of Myb-related proteins [19]. Despite the overall similarity there are differences that indicate that the SANT domain is functionally divergent from the canonical Myb DNA-binding domain [20]. SWIRM domain is a small alpha-helical domain of about 85 amino acid residues containing a helix-turn helix motif and binds to DNA [21]. Members of JAB family are found in proteasome regulatory subunits, eukaryotic initiation factor 3 (eIF3) subunits and regulators of transcription factors. This family is also known as the MPN domain [22] and PAD-1-like domain [23] JABP1 domain [24] or JAMM domain [25]. These are metalloenzymes that function as the ubiquitin isopeptidase/deubiquitinase in the ubiquitin-based signalling and protein turnover pathways in eukaryotes [25].
Orlistat as a FASN inhibitor and multitargeted agent for cancer therapy
Published in Expert Opinion on Investigational Drugs, 2018
Alejandro Schcolnik-Cabrera, Alma Chávez-Blanco, Guadalupe Domínguez-Gómez, Lucia Taja-Chayeb, Rocio Morales-Barcenas, Catalina Trejo-Becerril, Enrique Perez-Cardenas, Aurora Gonzalez-Fierro, Alfonso Dueñas-González
It is not surprising, after all, that many commonly altered oncogenes and tumor suppressor genes [5–11] activate both PI3K/AKT and ERK/MAPK signaling cascades, which activates the AKT/mTOR pathway that in turn leads to increased expression of positive regulators of FASN mRNA expression including sterol regulatory element binding protein-1c (SREBP-1c) and carbohydrate-activated transcription factor response element binding protein (ChREBP) [62,63]. There are additional transcriptional regulators of FASN gene, such as NAC1 [64], P300 acetyltransferase [65], the ubiquitous nuclear transcription factor Y (NF-Y) [65], and signaling via the GPER (G protein-coupled estrogen receptor) [66]. Moreover, in prostate cancer, FASN protein stabilization occurs via USP2a isopeptidase [67].