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Related to FASL: Fas protein, Fas receptor
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a substance (an atom or molecule or radical or ion) that forms a complex around a central atom

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Our molecular observations, showed no significant change in the expression of most pro- and anti-apoptotic genes in vitrified and non-vitrified groups, but the expression of Fas and FasL in the vitrified groups was significantly higher than the one in the non-vitrified groups.
According to the agreement, SBC grants to Cellect exclusivity to the FasL protein developed by SBC for a period of five years.
FITC-labeled FasL antibody (clone SB93a) was purchased from SouthernBiotech (Birmingham, USA), and FITC-labeled antibody to human MMP-9 (clone 56129) was purchased from R&D Systems (Minneapolis, USA); the corresponding mouse IgG2b kappa isotype control (clone eBMG2b) was obtained from eBioscience (Waltham, USA).
In line with these findings, significantly lower number of lung-infiltrated CD8 + CTLs expressing FasL (Figure 4(b)) and perforin (Figure 4(c)) was noticed in MSC +LLC1-treated mice when compared to LLC1-only treated animals indicating that systemic administration of MSCs suppressed both perforin- and FasL-mediated mechanisms of antitumor cytotoxicity of CTLs.
We observed the increase of FAS, FASL, and cleaved caspase-8 in the kidney of BDE-47-treated mice, while there was no significant change of procaspase-8 expression compared to control group (Figures 3(c) and 3(d)).
Cisplatin challenge stimulated overexpression of cytokines, and in the current study, we showed a significant increase in TNF[alpha], FasL, and IL1[beta] in the kidney tissues treated with cisplatin.
Zhang et al., "The serum miR-21 level serves as a predictor for the chemosensitivity of advanced pancreatic cancer, and miR-21 expression confers chemoresistance by targeting FasL," Molecular Oncology, vol.
Abbreviations: NSCLC, non-small cell lung cancer; MOMP, mitochondrial outer membrane permeabilization; PARP, poly (ADP-ribose) polymerase; Bax, Bcl-2-associated X protein; FasL, Fas ligand; FADD, Fas-associated protein with the death domain.
Apoptosis can be induced through either cytochrome c, Fasligand (FASL) or tumour necrosis factor (TNF) receptor 1-2, and endoplasmic reticulum activation.
The binding of TNF to its receptor causes the level of FasL to increase, which leads to the downstream activation of caspase 8.
The damage lead to release of pro-apoptotic molecules (FasL and TNF-[alpha]) which cause apoptosis and necrosis.
A description of many possible configurations can be found in (Fasl, 2013).
The book of Chahar Fasl (four-season) newspaper, by the effort of Fatahi, F., Tehran: Mostofi library.