CD95 _ FAS
- Known as:
- CD95 _ Fas Cell Surface Death Receptor
- Catalog number:
- GTX82928
- Product Quantity:
- 200 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
- Omega-3 fatty acids (omega-3 FAs) have been studied for the potential treatment of Atopic Dermatitis (AD). Dietary supplementation with omega-3 FAs may help in reducing AD symptoms, including the severity of lesions, inflammation, dryness, and pruritus. Nevertheless, because of their antiplatelet action, more cautious use of these supplements has been recommended in patients who have an invasive procedure or who are receiving antiplatelet or anticoagulant therapy. - Source: PubMed
Publication date: 2026/04/01
Abdul-Nabi Zainab Najim - Saline-alkaline stress, particularly sodium bicarbonate-induced alkaline stress, can cause tissue damage and oxidative stress in aquatic animals, thereby inhibiting their growth and even threatening their survival. This has become a key factor limiting the utilization of saline-alkaline water resources. This study for the first time systematically established acute and chronic time-series gradient NaHCO₃ stress treatments, and integrated histological observation, ultrastructural examination, enzyme activity determination as well as transcriptomic and metabolomic profiling to reveal the adaptive response mechanism of M. rosenbergii. - Source: PubMed
Publication date: 2026/06/16
Yu HengZou SongbaoLiu MeiNi MengJiang XiaoshanDeng MingfengYuan Julin - Prime editing is a versatile clinical genome editing method that enables precise substitutions, small insertions and deletions at specified locations in the genomes of living systems including human cells. Although non-viral lipid nanoparticle (LNP) delivery of RNA in vivo has become a preferred method for gene editing in animals and patients, its application to complex, three-component prime editing systems has yielded low editing efficiencies. Here we developed a systematic prime editing LNP (PE-LNP) optimization platform that addresses key bottlenecks in cargo design that limit editing efficiency. This generalizable workflow yielded PE-LNPs that can achieve 49% average in vivo prime editing in the bulk mouse liver with a single dose of 2 mg kg. We applied our workflow to the correction of PAH R408W, a cause of phenylketonuria, in a mouse model and achieved prime editing efficiencies and serum phenylalanine levels anticipated to be curative. We also show that PE-LNPs minimize off-target editing compared with DNA delivery methods, induce only transient elevation of liver enzymes and can be dosed repeatedly to improve editing efficiencies. These PE-LNP systems provide an attractive alternative to viral delivery by offering transient expression that minimizes off-target editing, no observed long-term toxicity and high levels of non-viral in vivo liver prime editing. - Source: PubMed
Publication date: 2026/06/15
Jiang Allen YCristian AnaBrooks Dominique LFeierman Emily RChen Paul ZWhittaker Madelynn NPierce Sarah ESakai Holt AChen HongyuLiu DangliangRandolph Peyton BLi Angus HHsu AlvinOmo-Lamai Serena OTao Y AllenOwusu-Amo BenistaWang XiaoWang XiaoMusunuru KiranLiu David R - Fas-associated phosphatase-1 (FAP-1), a nonreceptor protein tyrosine phosphatase, has been implicated in multiple signaling pathways, but its in vivo role remains unclear. Here, we show that FAP-1-deficient (FAP-1ΔP/ΔP) mice develop early megakaryocyte hyperplasia with defective platelet function and occasional hemorrhagic manifestations, accompanied by myelofibrosis-like features in aged animals. Bone marrow analysis revealed impaired demarcation membrane system (DMS) development with pre-DMS arrest in megakaryocytes, leading to defective proplatelet formation and impaired platelet function, with prolonged bleeding partly associated with reduced clot retraction. Mechanistically, FAP-1 deficiency induces sustained Src activation and cofilin inactivation, impairing perinuclear actin remodeling required for DMS expansion and resulting in pre-DMS arrest. With aging, approximately half of mice develop a symptomatic phenotype characterized by extramedullary hematopoiesis, hepatosplenomegaly, anemia, and thrombocytopenia; among these, most remain in a prefibrotic state, while a subset progresses to fibrosis-like changes. Bone marrow transplantation demonstrates that megakaryocyte abnormalities and fibrosis-associated changes are hematopoietic cell-intrinsic and partially transferable. Pharmacologic inhibition of Src with dasatinib attenuates these defects in FAP-1-deficient mice, supporting pathway specificity. In patients with primary myelofibrosis, reduced FAP-1 expression is associated with pre-DMS megakaryocyte accumulation, abnormal DMS and actin organization, and Src activation, supporting clinical relevance. Collectively, we identify a FAP-1-dependent mechanism governing Src-cofilin-mediated actin remodeling required for megakaryocyte maturation and platelet function, and suggest this pathway as a potential therapeutic target for platelet dysfunction, hemorrhagic complications, and fibrosis-associated disease. - Source: PubMed
Publication date: 2026/06/15
Chiu Mu-FanYeh Kun-HueiChen Pei-JerChou Wen-ChienLin Chung-WuChang KopingLin Chien-ChinYeh Shiou-Hwei - IntroductionDigital ulcerations and pre-ulcerative lesions are common in individuals with diabetes mellitus, peripheral neuropathy, and toe deformities. Flexor tenotomy has been recommended to assist in the healing of pre-ulcerative or ulcerative lesions with generally high rates of healing, although variable rates of complications have been reported. This study aimed to evaluate the safety, efficacy, and outcomes of flexor tenotomy for the treatment of pre-ulcerative and ulcerative digital lesions.MethodsA retrospective chart review was performed for patients who underwent percutaneous flexor tenotomy for treatment of digital ulcerations or pre-ulcerative lesions from January 2020 to January 2023. Outcomes assessed included healing of the index lesion and complications after tenotomy. Univariate analysis was performed to assess associations between clinical factors and outcomesResultsA total of 50 patients underwent flexor tenotomy, 25 for treatment of an ulceration and 25 for treatment of a pre-ulcerative lesion. The average length of follow-up was 786.32 days (range 36-1654 days). Healing of the index ulcer or pre-ulcerative lesion was noted in 92%. Transfer lesions were noted in 28%, of which 85.7% required a subsequent flexor tenotomy to address the secondary lesion/ulceration. No patients with prophylactic flexor tenotomy developed a transfer lesion.ConclusionThis study suggests the flexor tenotomy is a safe procedure with reliable rates of ulcer healing; however, it highlights a high risk of transfer lesions. Surgeons should remain vigilant for transfer lesions in the post-procedure period, and patients should be advised of the risk for transfer lesions after index flexor tenotomy.Levels of EvidenceLevel 4. - Source: PubMed
Publication date: 2026/06/15
Skolnik JenniferSpeis DarrahSciotti NicoleHossain MohammadMukhtar ZoreedSharma AanchalKigner StuartRose-Sauld SaraLandsman Adam