Interleukin 12B (natural killer cell stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40), CLMF, CLMF2, IL-12B, NKSF, NKSF2, rHuman Interleukin-12p40
- Known as:
- Interleukin 12B (natural killer cellular stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40), CLMF, CLMF2, Interleukin-12B, NKSF, NKSF2, rHuman Interleukin-12p40
- Catalog number:
- RF0031-10
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Agren
- Gene target:
- Interleukin 12B (natural killer cell stimulatory factor 2 cytotoxic lymphocyte maturation p40) CLMF CLMF2 IL-12B NKSF NKSF2 rHuman Interleukin-12p40
Related genes to: Interleukin 12B (natural killer cell stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40), CLMF, CLMF2, IL-12B, NKSF, NKSF2, rHuman Interleukin-12p40
- Gene:
- ARMH1 NIH gene
- Name:
- armadillo like helical domain containing 1
- Previous symbol:
- NCRNA00082, C1orf228
- Synonyms:
- MGC33556, p40
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 2008-09-02
- Date modifiied:
- 2019-02-21
- Gene:
- ARPC1B NIH gene
- Name:
- actin related protein 2/3 complex subunit 1B
- Previous symbol:
- -
- Synonyms:
- ARC41, p40-ARC, p41-ARC
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-06
- Date modifiied:
- 2019-04-23
- Gene:
- CD7 NIH gene
- Name:
- CD7 molecule
- Previous symbol:
- -
- Synonyms:
- GP40, LEU-9, TP41, Tp40
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- DNAJB1 NIH gene
- Name:
- DnaJ heat shock protein family (Hsp40) member B1
- Previous symbol:
- HSPF1
- Synonyms:
- Hsp40, Sis1, RSPH16B
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2015-11-19
- Gene:
- EIF3H NIH gene
- Name:
- eukaryotic translation initiation factor 3 subunit H
- Previous symbol:
- EIF3S3
- Synonyms:
- eIF3-gamma, eIF3-p40, eIF3h
- Chromosome:
- 8q23.3-q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-26
- Date modifiied:
- 2018-02-13
Related products to: Interleukin 12B (natural killer cell stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40), CLMF, CLMF2, IL-12B, NKSF, NKSF2, rHuman Interleukin-12p40
Related articles to: Interleukin 12B (natural killer cell stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40), CLMF, CLMF2, IL-12B, NKSF, NKSF2, rHuman Interleukin-12p40
- Little is known about the in-vivo dynamics of biofilms associated with medical-device infections and their interplay with systemic inflammation, local immune responses, and tissue healing processes. There may be an opportunity to tailor therapeutic strategies to target these dynamics to improve treatment outcomes. We investigated immune responses to a methicillin-susceptible (ATCC 12600) and a multi-drug resistant (L1101) S. aureus strain using a rat subcutaneous implant model, analyzing local and systemic inflammation through 19 gene expressions over 21 days. Our goals were to identify differences in the immune response due to infection and also with respect to the two strains. We observed that systemic inflammation, indicated by α-2-macroglobulin, was elevated in the initial stages (up to day 7). Local inflammatory cytokine levels (IL-6, TNF-α, IL-6, TNF-α, IL-1β, IL10, IL-17, IL12a, IL12b, IFNG) varied by strain, typically higher against the clinical strain. Infections generally hindered early macrophage (MCSF1) and T-cell (CD4, CD5, CD6, CD8A) recruitment, particularly in cases involving the clinical strain. Conversely, a better healing response was observed in the infection of the more susceptible ATCC 12600 strain (VEGF, CXCR1, CXCR2, MMP-1, MMP-3, MMP-13). These results are crucial for understanding immune responses to such infections, guiding therapeutic strategies. - Source: PubMed
Publication date: 2025/04/17
Fan YingfangSekar AmitaMcCanne MadelineYuh JeanKannambadi Devika DuttaLekkala SashankMuratoglu Orhun KOral Ebru - Suppression within the tumor microenvironment (TME) hampered natural killer (NK) cells and their role in cancer immunotherapy. This study explores how interleukin (IL) signaling (IL-12A, IL-12B, IL-15, IL-18) and interferon gamma (IFNG or IFN-γ) interact with microRNAs to regulate NK cell function in cancer. - Source: PubMed
Zabeti Touchaei ArefehVahidi SogandSamadani Ali Akbar - Interleukin-12 (IL12) plays a crucial role in immune regulation and inflammation and is critical in developing colorectal cancer (CRC). This study investigated the association between rs568408, rs2243115, and rs3212227 polymorphisms and CRC susceptibility in a Taiwanese population. - Source: PubMed
Yueh Te-ChengChen Ying-JingMong Mei-ChinKe Tao-WeiShih Hou-YuWang Yun-ChiChang Wen-ShinBau DA-TianTsai Chia-Wen - The presentation of posterior ocular tuberculosis (TB) varies greatly along with the need for immunomodulatory therapy to control inflammation. In this study, we explore the potential mechanisms and pathways for autoimmune-related inflammation in ocular TB using molecular mimicry-based mathematical modeling. - Source: PubMed
Publication date: 2024/12/30
Kutlutürk Karagöz IşılKaya MücahitKıvrak UlviyeMunk Marion R - This study investigates the role of NIK in activating specific inflammatory genes in macrophages, focusing on the effect of a mutation in NIK found in alymphoplasia (/) mice. Mouse peritoneal macrophages from / mice showed a severe defect in the production of some pro-inflammatory cytokines, such as IL-12. This effect seemed to take place at the transcriptional level, as shown by the reduced transcription of and in / macrophages after exposure to the TLR4 agonist LPS. Immunoprecipitation studies showed that the binding of NIK to c-Rel was not efficient in RAW 264.7 cells over-expressing the / mutation. In addition, the shuttling of c-Rel to the nucleus was shown to be impaired in / macrophages in response to LPS. When looking more specifically at the regulation of the promoter, we found that c-Rel bound to the NF-kB consensus sequence in macrophages from WT mice 1 hr. after LPS challenge, whereas in / macrophages, the transcription factor bound to the promoter was p65. These findings indicate that NIK is essential for efficient c-Rel activation and proper inflammatory responses. NIK dysfunction could lead to weakened immune responses, and targeting this pathway may help in developing therapies for immune-related conditions. - Source: PubMed
Publication date: 2025/01/03
Cuesta NataliaStaniszewska Anna DMoreno CristóbalPunzón CarmenFresno Manuel