CD95 _ FAS
- Known as:
- CD95 _ Fas Cell Surface Death Receptor
- Catalog number:
- GTX13549
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD95 _ FAS
Related genes to: CD95 _ FAS
- Gene:
- FAS NIH gene
- Name:
- Fas cell surface death receptor
- Previous symbol:
- FAS1, APT1, TNFRSF6
- Synonyms:
- CD95, APO-1
- Chromosome:
- 10q23.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-25
- Date modifiied:
- 2019-04-23
Related products to: CD95 _ FAS
Related articles to: CD95 _ FAS
- Macrophages represent an essential component of the innate immune system that regulates multiple nervous system functions. This is highlighted in previous research that identifies an important somatosensory role for macrophages in peripheral dorsal root ganglia (DRG). In several pre-clinical pain models, DRG macrophage numbers increase with little evidence as to the origin. The objective of this work was to investigate this phenomenon with the innovative Macrophage Fas-Induced Apoptosis (MaFIA) mouse transgenic animal model and establish the source of macrophage expansion in a chronic intermittent hypoxia model. Intrathecal administration of AP20187 was performed in MaFIA mice to take advantage of the blood brain barrier impermeability of AP20187 and prevent exposure to systemic tissues in order to determine whether knocking down DRG tissue resident macrophages would alter hypoxia-related doubling of cell numbers in DRG. Localized AP20187 exposure to the central nervous system and adjacent DRG structures reduced macrophage in restricted neuronal tissues including spinal column and DRG without affecting macrophage populations in bone marrow, circulating blood, and sciatic nerve. Furthermore, MaFIA mice treated with AP20187 produced no increase in DRG macrophage cell numbers following exposure to chronic intermittent hypoxia. These findings indicate that targeted intrathecal administration of AP20187 reduces DRG tissue-resident macrophages and prevents chronic intermittent hypoxia-induced expansion of the innate immune cell population, negating a role for circulating monocytes in the phenomenon. - Source: PubMed
Publication date: 2026/08/17
Chivers Samuel BMcLay Cassandra LJeske Nathaniel A - Early revision of primary Achilles tendon repair is sometimes necessary, and the Achilles tendon's inherent hypovascularity creates a uniquely challenging biological environment for reoperation. However, the optimal timing for revision and its associated complication risks remain poorly characterized. - Source: PubMed
Publication date: 2026/08/17
Cherelstein Rachel EKotapati SamhitaAlkaramany EslamRodriguez-Materon Solangel - Depletion of calcium from ER stores leads to the activation of calcium channels on the plasma membrane known as store-operated calcium entry. The proteins STIM1 and STIM2 function as ER calcium sensors, and upon store depletion, they undergo a conformational change that allows them to bind to and gate Orai calcium channels on the plasma membrane. We have shown that both Orai1 and STIM1 are dynamically S-acylated after store depletion, which is required for SOCE. These results suggest the requirement of a calcium-activated protein S-acyltransferase (PAT) such as DHHC21. Here, we show that DHHC21 is essential for SOCE in vitro and in vivo. Using the depilated mouse model that expresses DHHC21 but cannot be activated by calcium, we show that DHHC21 activation is a major mediator of STIM1 S-acylation and subsequent calcium entry. Plasma membrane-localized DHHC21 is dynamically recruited into Orai1/STIM1 puncta upon store depletion, where it physically binds to STIM1. Finally, we show that depilated mice phenocopy many aspects of autoimmune lymphoproliferative syndrome (ALPS), including defective Fas-mediated calcium release, T cell death, neutropenia, and increased serum vitamin B12 levels. Targeting DHHC21 may be therapeutically beneficial for ALPS and diseases associated with deregulated activation of STIM1, such as tubular aggregate myopathy and Stormorken syndrome. - Source: PubMed
Publication date: 2026/08/17
Kodakandla GouthamFan YingZhu Michael XWest Savannah JAkimzhanov AskarBoehning Darren - The aim of this study was to describe and compare the fatty acid (FA) profiles of hepatic tissue in farmed and wild channel catfish (, Rafinesque, 1818). Thirty-four liver samples were collected from farmed and wild channel catfish. After FA samples were extracted, their fatty acid profiles were obtained by gas chromatography with a flame ionization detector (GC-FID). The analysis revealed that monounsaturated FAs were present at higher concentrations in farmed organisms (161.45 mg/100 g) than in wild organisms (46.87 mg/100 g). While the most abundant FA group in wild organisms was saturated FAs (58.48 mg/100 g), farmed catfish had higher levels (73.22 mg/100 g). The farmed organisms also presented a higher total concentration of FA (296.03 mg/100 g), which is double the mean obtained in wild channel catfish (131.89 mg/100 g). Nonsignificant differences were found in the polyunsaturated, omega-3 and omega-6 quantities, yet a suggestive difference was found for EPA. Our findings suggest that the fatty acid content in the liver is notably different between wild and farm origins. The differences identified in this study were attributed to differential feeding patterns in the analyzed populations of farmed and wild channel catfish. - Source: PubMed
Publication date: 2025/12/20
Esparza-Acebo Leilany MargaritaPerales-Torres Adriana LeticiaDe la Rosa-Reyna Xochitl FabiolaRodríguez-Castillejos Guadalupe ConcepciónEsquivel Aldo VegaMontelongo-Alfaro Isidro OtonielBenavides-González FlavianoParra-Bracamonte Gaspar Manuel - Reducing dietary nutrient density may lower the feed cost but compromise the growth performance in piglets. Given the ability of lysolecithin (LPI) to enhance nutrient utilization, its supplementation may help piglets adapt to a low-nutrient (LN) diet. This study aimed to investigate the effects of dietary LPI supplementation on growth performance, nutrient utilization, metabolism, and muscle development in piglets fed a LN diet. A total of 96 nursery piglets (17.0 ± 0.2 kg in initial body weight [BW] and 50 d of age) were randomly assigned to three groups in a randomized complete block design and received either the normal-nutrient diet (CON), a LN diet, or the LN diet supplemented with 400 mg/kg lysolecithin (LN-LPI) for 28 d. Each dietary treatment included 8 replicates of 4 piglets each. Results showed that the LN-LPI diet improved the average daily gain (ADG; = 0.040) during the first two weeks, feed-to-gain ratio (F:G; = 0.032), and BW ( = 0.065) throughout the experimental period, reaching levels comparable to those of piglets in the CON group. Compared with the LN diet, the growth-promoting effect of LPI may be attributed to its role in increasing the digestibility of ether extract (EE; < 0.001) and gross energy (GE; = 0.022) in diets, as well as increasing the relative weight of psoas major muscles (PMM) and the EE ( = 0.049) and crude protein (CP) content ( = 0.007) in muscle. Accordingly, compared with the LN diet, LPI supplementation decreased the blood urea nitrogen ( = 0.003) and total cholesterol (TC) concentrations ( = 0.017), and increased total superoxide dismutase (T-SOD) levels in plasma ( = 0.005) and liver ( = 0.006), along with the lower malondialdehyde (MDA) levels in blood ( < 0.001) and liver ( = 0.003). In addition, microarray analysis indicated that dietary LPI supplementation promoted expression of lipid synthesis and transport-related genes in the liver (, = 0.040; , = 0.001; and , = 0.025), and amino acid (AA) transport and synthesis-related genes (, = 0.021; , = 0.004), compared with the LN diet in muscle. In conclusion, this study demonstrated that the LN-LPI diet mitigated the compromised growth performance commonly observed under nutrient restriction, potentially mediated by improving nutrient utilization and redox status, and modulating lipid and protein metabolism. - Source: PubMed
Publication date: 2026/06/08
Song HuaqiZhang ZhimingYao RenjieZhou QiangLiu YangJin JinJin JunqiLuo ZhengTang JiayongFeng BinXu ShengyuLin YanHua LunZhuo YongWu DeChe Lianqiang