Human Cellexp Human Recombinant IL-6 proteins
- Known as:
- Human Cellexp Human Recombinant Interleukin-6 proteins
- Catalog number:
- 6464-50
- Product Quantity:
- 50
- Category:
- Proteins
- Supplier:
- Biovis
- Gene target:
- Human Cellexp Recombinant IL-6 proteins
Ask about this productRelated genes to: Human Cellexp Human Recombinant IL-6 proteins
- Gene:
- CEBPB NIH gene
- Name:
- CCAAT enhancer binding protein beta
- Previous symbol:
- TCF5
- Synonyms:
- LAP, CRP2, NFIL6, IL6DBP, C/EBP-beta
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-02-27
- Date modifiied:
- 2018-02-23
- Gene:
- CEBPD NIH gene
- Name:
- CCAAT enhancer binding protein delta
- Previous symbol:
- -
- Synonyms:
- CRP3, CELF, C/EBP-delta, NF-IL6-beta
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-24
- Date modifiied:
- 2018-02-23
- Gene:
- ENTPD6 NIH gene
- Name:
- ectonucleoside triphosphate diphosphohydrolase 6
- Previous symbol:
- CD39L2, IL6ST2
- Synonyms:
- NTPDase-6, dJ738P15.3
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2019-02-28
- Gene:
- IL6 NIH gene
- Name:
- interleukin 6
- Previous symbol:
- IFNB2
- Synonyms:
- IL-6, BSF2, HGF, HSF
- Chromosome:
- 7p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-12
- Gene:
- IL6RP1 NIH gene
- Name:
- interleukin 6 receptor pseudogene 1
- Previous symbol:
- IL6RL1
- Synonyms:
- -
- Chromosome:
- 9q22.2
- Locus Type:
- pseudogene
- Date approved:
- 1991-08-18
- Date modifiied:
- 2014-11-19
Related products to: Human Cellexp Human Recombinant IL-6 proteins
Related articles to: Human Cellexp Human Recombinant IL-6 proteins
- Interleukin-6 (IL-6) stands as a therapeutically important target, and the efficient chemical synthesis of mirror-image D-IL-6 could facilitate the development of D-peptide antagonists to complement the existing repertoire of antibody-based antagonists. Herein, we report a new integrated synthetic strategy for D-IL-6 characterized by three key features: a three-segment assembly of full-length D-IL-6 via two ligation reactions; a one-pot process of low-energy visible light-induced desulfurization and acetamidomethyl (Acm) deprotection; and the mitigation of poor intermediate solubility using organic cosolvents. By minimizing operational steps, this streamlined approach enhances the overall yield of D-IL-6 synthesis compared to the previous methods and establishes a robust platform for the discovery of IL-6-targeting D-peptide therapeutics. - Source: PubMed
Publication date: 2025/09/17
Ren YuxiangLiu YanboHan DongyangLiang Lu-Jun - Interleukin-6 (IL-6) plays a crucial role in regulating of survival, invasion, and cell cycle of breast cancer cells. So, it appears that the suppression of IL-6 may function as a potential therapeutic agent in the context of cancer treatment. The aim of the present study is to investigate the effect of a mutated form of the soluble IL-6 receptor (mIL-6R) on the invasive ability and induction of apoptosis in MDA-MB-231 cancer cells. - Source: PubMed
Publication date: 2025/09/17
Mousavizadeh-Marvast Maryam SadatMirian MinaShafiee Fatemeh - Allergic conjunctivitis (AC) is an IgE-mediated type I hypersensitivity disorder characterized by conjunctival hyperemia, itching, and increased tear secretions. This study aims to investigate the mechanism of FOXP3 in the inflammatory activation of human conjunctival epithelial cells (HConEpiCs) in AC. Serum samples were collected from AC patients and healthy volunteers for correlation analysis of FOXP3 with inflammatory cytokines (IL-6/IL-8/TNF-α/CRP) and immunoglobulins (IgG/IgA/IgE). FOXP3, KAT5, and PDCD4 expression were measured by RT-qPCR, followed by Pearson correlation analysis. HConEpiCs were used to establish an AC cell model, followed by assessment of cell viability and inflammatory cytokines (IL-6/IL-8/TNF-α/IL-10/IL-4). The binding of FOXP3 to the KAT5 promoter and KAT5 and H3K27ac enrichment on the PDCD4 promoter were detected. FOXP3 expression was downregulated in AC patient, while KAT5 and PDCD4 were upregulated. FOXP3 negatively correlated with IL-6, IL-8, TNF-α, C-reactive protein, serum IgG, IgA, IgE, and eosinophil ratio. In histamine-stimulated HConEpiCs, FOXP3 overexpression inhibited inflammation. Mechanistically, FOXP3 bound to the KAT5 promoter to inhibit KAT5 expression, reduced KAT5 and H3K27ac enrichment on the PDCD4 promoter, and downregulated PDCD4 expression. KAT5 or PDCD4 overexpression reversed FOXP3-mediated inhibition of HConEpiC inflammatory activation. In conclusion, FOXP3 overexpression attenuates inflammatory activation of HConEpiCs by inhibiting KAT5 expression and reducing KAT5/H3K27ac-mediated PDCD4 transcription. - Source: PubMed
Publication date: 2025/09/17
Deng Zifeng - Caveolae and Rho kinase signaling individually are both remodeled during cellular senescence and influence cell morphology and SASP secretion. However, how this interaction modulates senescent cancer-cell morphology and SASP remains unresolved. We evaluated the possible connection between caveolae and ROCK on the development of senescent cell morphology and the secretion of the SASP. - Source: PubMed
Publication date: 2025/09/17
Şimay Demir Yaprak DilberMohammed Ahmed IslamÖzdemir AysunArk Mustafa - Hepatitis E virus infection typically results in a self-limited acute viral hepatitis (AVH-E), which is rapidly cleared by the host immune response. In this longitudinal study, temporal cytokine and chemokine profiles were analysed in AVH-E patients' sera using a multiplex immunoassay. HEV RNA became undetectable between 9 and 18 days, with a median of 13 days, occurring 3-20 days after symptom onset. In the AVH-E group, IFN-γ peaked significantly around days 6-9, which is prior to the HEV RNA clearance period, and declined during days 9-18. IL-2, IL-10, and TNF-α increased significantly during days 15-20, while IL-1β and IL-6 showed peak levels. CCL3, CXCL6, CXCL9, CXCL10 and MIF were significantly higher in the AVH-E group than in the healthy controls; CCL2 and CCL20 peaked non-significantly during days 12-17. CCL3, CXCL6, CXCL9 and CXCL10 levels were lower in the AVH-E group than in the AVH-B group. Compared to the AVH-B group and healthy controls, the AVH-E group showed distinct immune signatures. These findings highlight coordinated cytokine and chemokine responses during HEV infection and provide insights into the immunopathogenesis of self-limiting hepatitis E. - Source: PubMed
Bhatia PoojaMohd AasKatiyar HarshitaGoel AmitAggarwal RakeshVeerapu Naga Suresh