IL_29 (human) Singleplex MultiBead Kit
- Known as:
- IL_29 (H. sapiens) Singleplex MultiBead Kit
- Catalog number:
- ASA985-025
- Product Quantity:
- 96 Well
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- IL_29 (human) Singleplex MultiBead Kit
Related genes to: IL_29 (human) Singleplex MultiBead Kit
- Gene:
- IFNL1 NIH gene
- Name:
- interferon lambda 1
- Previous symbol:
- IL29
- Synonyms:
- IL-29
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-02
- Date modifiied:
- 2016-10-11
Related products to: IL_29 (human) Singleplex MultiBead Kit
Related articles to: IL_29 (human) Singleplex MultiBead Kit
- SARS-CoV-2 portrays a public health threat because severe progression of infections can lead to hospitalization. Severity is often characterized by a systemic inflammatory response in later stages, along with disbalance in cytokine production, multi-organ failure, or acute respiratory distress syndrome (ARDS). As severe infections can be challenging due to limited treatment windows for direct-acting antivirals, host-targets, e.g., the Raf/MEK/ERK signaling cascade, came into focus. Specifically, MEK1/2 has been suggested as a target for antiviral and anti-inflammatory therapy. A recent phase II clinical trial showed the efficacy of the MEK1/2 inhibitor zapnometinib (ZMN/ATR-002) in hospitalized COVID-19 patients. The anti-inflammatory action of ATR-002 was only studied on some candidate cytokines. - Source: PubMed
Publication date: 2026/05/29
Rodner FranziskaSchughart KlausLudwig StephanSchreiber André - Rift Valley fever virus (RVFV) is a mosquito-borne Phlebovirus and zoonotic pathogen affecting maternal-fetal health. Vertical transmission is linked to miscarriage and severe fetal outcomes, but mechanisms of placental pathogenesis remain unclear. We used first-trimester human trophoblast stem cells (hTSCs) to model infection at the maternal-fetal interface. Immunofluorescence, qRT-PCR, western blotting, and single-cell transcriptomics showed that hTSCs are highly susceptible to RVFV. Strand-specific viral transcriptomics confirmed the ambisense S segment and revealed preferential transcription of the M and S segments over L. RVFV induced G1 arrest, impairing trophoblast proliferation and differentiation, and drove widespread transcriptional reprogramming, including strong interferon lambda 1 () but modest type I interferon responses, and dysregulation of inflammatory and preeclampsia-associated genes such as and . Recombinant IFN-λ pretreatment reduced RVFV protein expression, highlighting hTSCs as a robust model and IFN-λ as a promising antiviral strategy. - Source: PubMed
Publication date: 2026/04/03
Gwon Yong-DaeHaider SandraKnöfler MartinBradley MatthewHenriksson JohanEvander Magnus - Glioblastoma (GBM) is an aggressive tumor with limited therapeutic options. Zika virus (ZIKV) has demonstrated activity against GBM; however, the cellular pathways behind this interaction remain unclear. We systematically reviewed open-access primary studies assessing differentially expressed genes (DEGs) in GBM models infected with wild-type or engineered ZIKV using transcriptomic approaches (inclusion criteria); reviews, restricted-access studies, commentaries, preprints, abstracts, and articles lacking data or not meeting these conditions were excluded (PROSPERO CRD420251077092). We performed a pathway analysis of reported DEGs. PubMed and Google Scholar were searched up to 5 March 2025; 139 records were identified and 5 met the eligibility criteria. Risk of bias was evaluated using an adapted ToxRTool for in vitro experiments and the SYRCLE RoB tool for in vivo models. Altogether, 4360 genes were reported as upregulated and 2072 as downregulated; 12 genes (, , , , , , , , , , , and ) were consistently upregulated, none were consistently downregulated. Pathway analysis of the studies providing complete DEG lists identified 23 commonly enriched pathways mostly related to interferon signaling. These findings may help guide future research in this field; nevertheless, methodological heterogeneity limits comparability, reinforcing the need for standardized protocols. Funding: ITpS, CNPq, and FAPEMIG. - Source: PubMed
Publication date: 2026/02/15
Menezes DiegoReis Clarisse RezendeMamede IzabelaGeddes Victor Emmanuel Vianade Souza Renan PedraAguiar Renato Santana - Viral myocarditis (VMC) is a myocardial injury syndrome caused by enterovirus infections, including Coxsackievirus B5 (CVB5) and Echovirus 6 (ECHO6). However, the exact pathogenesis of VMC by enteroviruses remains unclear. Here, the host immune response differences in transcriptomics in human cardiomyocyte AC16 cells upon CVB5 and ECHO6 infections were explored. CVB5 and ECHO6 effectively infected AC16 cells, showing significant viral replication and cytopathic effects at 48 h post-infection. Transcriptomic analysis indicated that both CVB5 and ECHO6 infection induced a series of immune- and inflammation- related genes, including IL6, CCL3, and IFNL1, which were validated by qPCR. Additionally, Ribavirin demonstrated a certain inhibitory effect on the viral replication of both CVB5 and ECHO6 at a concentration of 50 µm. This study established a systematic comparison of the common transcriptomic differences and immune response characteristics of both CVB5 and ECHO6 infection in human cardiomyocytes. The marked upregulation of immune-related genes suggests that innate immunity and the inflammatory response play critical roles in cardiomyocytes defense against enterovirus infection. Ribavirin showed notable inhibitory activity against both CVB5 and ECHO6. The study sheds light on new insights into the foundations for the pathogenesis of enterovirus-associated VMC and the development of promising therapeutic approaches against VMC. - Source: PubMed
Xu YiLan XianwuChen JianweiYou JieyuKo Hiu TungFang ChuqunCui ShanshanShereen Muhammad AdnanLuo ZhenWu Shaorong - TANK-binding kinase 1 (TBK1) acts at the crossroads of various host immune pathways. Autosomal dominant (AD) and recessive (AR) TBK1 deficiencies have been reported in human patients with herpes simplex encephalitis and SARS-CoV-2 pneumonia (AD deficiency) or systemic inflammation (AR deficiency). We describe here a Turkish boy, born to consanguineous parents and homozygous for a loss-of-function mutation of , who had experienced recurrent vesicular skin eruptions presumably triggered by herpesviral infection and five episodes of viral pneumonia since the age of 2 mo. Whole-exome sequencing identified a biallelic mutation of the gene (: c.922C>T, p.Arg308Ter). The induction of , , , and was abolished or severely impaired in SV40-fibroblasts from the patient following stimulation of the TLR3 or RIG-I/MDA5-RIG-I pathways. The patient underwent stem-cell transplantation, but unfortunately succumbed to suspected post-viral acute disseminated encephalomyelitis at the age of 2.5 years. AD or AR TBK1 deficiency should be considered in patients with severe viral infections. - Source: PubMed
Publication date: 2025/12/03
Kilic Sara SebnemZhao ShuxiangLiu ZhiyongKarali YasinYalcin KorayBodansky AaronChakravarty DebanjanaWilson MichaelCasanova Jean-LaurentZhang Shen-Ying