Anti-Rat CD8b FITC 500 ug
- Known as:
- Antibody toRat CD8b fluorecein 500 ug
- Catalog number:
- 11-0080-85
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Rat CD8b FITC 500
Related genes to: Anti-Rat CD8b FITC 500 ug
- Gene:
- CD8B NIH gene
- Name:
- CD8b molecule
- Previous symbol:
- CD8B1
- Synonyms:
- -
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-13
- Date modifiied:
- 2016-10-05
Related products to: Anti-Rat CD8b FITC 500 ug
Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodies"MANTLE 500 ML 2"" HOLE " Prod. Code Pα - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(-)-Epigallocatechin gallate (EGCG)(-)-Scopolamine Perchlorate (Hyoscine perchlorate)(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS: Related articles to: Anti-Rat CD8b FITC 500 ug
- Compared with transplanted tumors, autochthonous tumors are difficult to cure using experimental radiation therapy in mice. Here we analyzed differences in immune-related gene expression profiles between mouse fibrosarcomas subcutaneously induced by 3-methylcholanthrene (3MC) and their corresponding transplanted tumors. The immune genes examined were Pd1, Pdl1, Pdl2, Cd3d, Cd8a, Cd8b, Ifnγ, Itga2, Gzmb, and Foxp3. Among 12 tumors, one was non-transplantable and showed a benign phenotype with an abundance of DX5+ natural killer cells and CD8+ T cells together with increased IFNγ expression and mRNA levels of all immune genes except for Itga2. The other 11 transplantable tumors showed increased expression of Pd1, Pdl1, Pdl2, Cd3d, Cd8b, and Ifnγ following transplantation into syngeneic mice. These effects of transplantation highlight the relevance of immune gene expression status to the curability of tumors. - Source: PubMed
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Publication date: 2026/02/13
Ben Abdallah HakimDaugaard ChristineSchøsler LouiseRasmussen Mads KirchheinerKibsgaard LineHøgsberg TrineJohansen ClausBertelsen Trine - Postoperative cognitive dysfunction is a type of cognitive impairment that occurs after surgery. Here, this experiment investigated the role of PLCG1 in sevoflurane-induced model and the molecular mechanisms underlying its regulation of ferroptosis. Single-cell RNA sequencing data and bioinformatic analyses were performed using GEO datasets (GSE196239). Mice were exposed to 2.3% sevoflurane for 2 h daily for 3 consecutive days. PLCG1 expression was up-regulation in patients exposed to sevoflurane. Specifically, blood samples from these patients exhibited elevated levels of PLCG1 mRNA. Consistently, in a mouse model of sevoflurane exposure, both mRNA and protein levels of PLCG1 were significantlyincreased in brain tissue. Single-cell RNA sequencing analysis revealed that PLCG1 was predominantly expressed in astrocytes (marked by AQP4, GFAP, LUZP2, and SLC25A28) and neurons (marked by B3GAT2, ENO2, GNG2, and SLC1A1) in sevoflurane-exposed patients. In contrast, PLCG1 expression was undetectable in B cells (CD74, CD79B, CD80, CD86), T cells (CD4, CD8B, CD69, CD247), or macrophages (CD36, CD68, CD83, CD163). In conclusion, PLCG1 drives neuronal ferroptosis in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. In conclusion, PLCG1 drives neuronal in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A Ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. - Source: PubMed
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