RIPK1 polyclonal antibody (A01)
- Known as:
- RIPK1 pab (anti-) (A01)
- Catalog number:
- H00008737-A01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- RIPK1 polyclonal antibody (A01)
Related genes to: RIPK1 polyclonal antibody (A01)
- Gene:
- ABRAXAS2 NIH gene
- Name:
- abraxas 2, BRISC complex subunit
- Previous symbol:
- KIAA0157, FAM175B
- Synonyms:
- Em:AC068896.4, ABRO1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2017-04-27
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
- Gene:
- ARHGAP4 NIH gene
- Name:
- Rho GTPase activating protein 4
- Previous symbol:
- -
- Synonyms:
- KIAA0131, C1, p115, RhoGAP4, SrGAP4
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2015-09-11
- Gene:
- ARHGEF7 NIH gene
- Name:
- Rho guanine nucleotide exchange factor 7
- Previous symbol:
- -
- Synonyms:
- KIAA0142, PIXB, DKFZp761K1021, Nbla10314, DKFZp686C12170, BETA-PIX, COOL1, P85SPR, P85, P85COOL1, P50BP, PAK3, P50
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2016-10-05
- Gene:
- BCLAF1 NIH gene
- Name:
- BCL2 associated transcription factor 1
- Previous symbol:
- -
- Synonyms:
- KIAA0164, BTF
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2017-06-09
Related products to: RIPK1 polyclonal antibody (A01)
Related articles to: RIPK1 polyclonal antibody (A01)
- The cGAS-STING1 pathway is essential for innate immunity, while its functions beyond immune activation have emerged as a key research topic. Recent studies have revealed the non-canonical roles of this pathway in autophagy. However, whether it participates in organelle quality control through selective autophagy processes such as mitophagy remains largely unexplored. In our study, we identify the cGAS-STING1 pathway as an essential upstream regulator of PINK1-PRKN-dependent mitophagy. We demonstrate that upon mitochondrial damage, STING1 is recruited to damaged mitochondria in a process requiring PINK1- and VCP/p97-mediated degradation of outer mitochondrial membrane proteins. STING1 at damaged mitochondria then activates TBK1, which phosphorylates the mitophagy receptor OPTN at Ser177, enhancing its recruitment to damaged mitochondria and driving efficient mitophagy. Disruption of the STING1-TBK1-OPTN axis impairs mitophagy and shifts the cellular response from pro-survival mitophagy to apoptosis. Our findings therefore uncover a non-canonical, pro-survival function of the cGAS-STING1 pathway in mitophagy, extending its role beyond innate immunity to the regulation of selective autophagy and cell fate decisions. Abbreviations: BafA1: bafilomycin A1; cGAS: cyclic GMP‑AMP synthase; ER: endoplasmic reticulum; GABARAP: GABA type A receptor-associated protein; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MQC: mitochondrial quality control; mtDNA: mitochondrial DNA; NAC: N-Acetylcysteine; Nec-1: Necrostatin-1; OMM: outer mitochondrial membrane; OPTN: optineurin; PINK1: PTEN induced kinase 1; PRKN: parkin RBR E3 ubiquitin protein ligase; RIPK1: receptor interacting serine/threonine kinase 1; ROS: reactive oxygen species; STING1: stimulator of interferon response cGAMP interactor 1; TBK1: TANK binding kinase 1; TFEB: transcription factor EB; VCP/p97: valosin containing protein; Z-VAD-FMK: benzyloxycarbony (Cbz)-l-ValAla-Asp (OMe)-fluoromethylketone. - Source: PubMed
Publication date: 2026/06/13
Huang Ze-BoLin Jin-YiCheng Ling-JunTan Hayden Weng SiongShen Han-MingLu Guang - Cyclophosphamide (CTX) is widely used in chemotherapy; however, its clinical application is frequently accompanied by gonadotoxic effects, which can result in impaired ovarian function and subsequent infertility in women. Consequently, effective strategies to mitigate chemotherapy-induced ovarian injury remain an important unmet need. Interleukin-35 (IL-35), a recently identified member of the IL-12 cytokine family, has been implicated in immune regulation and the maintenance of immune homeostasis. In parallel, accumulating evidence indicates that ovarian damage involves multiple forms of regulated cell death rather than a single apoptotic pathway. PANoptosis, an integrated cell-death program encompassing pyroptosis, necroptosis, and apoptosis, has recently emerged as a key mechanism in tissue injury. To date, whether IL-35 participates in CTX-induced ovarian injury and whether it modulates PANoptosisrelated pathways has not been clearly elucidated. - Source: PubMed
Publication date: 2026/06/09
Zhang YuhanZhou WeiYu JiaZhong YuanZhao YanChen Qi - Cell death is a fundamental biological process with critical roles in both normal physiology and pathological conditions, especially programmed cell death, such as apoptosis, necroptosis and pyroptosis. Programmed cell death is mediated by cascade signaling transduction rely on protein-protein interaction. Necroptosis mediator RIPK1, RIPK3 and MLKL have been shown to be regulated by different types of post-translational modifications (PTMs), suggesting that additional factors must associate with them during necroptosis. Proximity labeling (PL) has been used to tag and identify proteins, RNAs, or other biomolecules in close proximity (∼10-20 nm) to a target protein of interest. Therefore, utilizing proximity labeling coupled mass spectrometry to identify weak and transient interactors of necroptosis mediators, will be helpful for the further understanding of cell death mechanisms and functions. Here, in this chapter, we provide a step-by-step protocol for using TurboID-based proximity labeling to map interactors and regulators of key necroptotic proteins (RIPK1, RIPK3, MLKL and ZBP1). - Source: PubMed
Publication date: 2026/03/03
Hua JiangChan Francis Ka-Ming - The generation of isogenic knockout (KO) cell lines for intracellular proteins using non-viral CRISPR-Cas9 approaches has long been technically demanding and time-consuming. Here, we describe a streamlined and cost-effective method based on ptARgenOM, an all-in-one mammalian expression vector designed for efficient delivery of the CRISPR-Cas9 system. This vector co-expresses the guide RNA (gRNA) and Cas9 endonuclease, which is fused to a ribosomal skipping peptide sequence followed by the enhanced green fluorescent protein (EGFP) and the puromycin N-acetyltransferase. This design enables transient, expression-dependent antibiotic selection and fluorescence-based enrichment of successfully transfected cells, facilitating the rapid generation of isogenic KO populations or clones. The method is particularly well-suited, though not limited, to functional studies involving intracellular components of the cell death machinery, including both the extrinsic and intrinsic apoptotic signaling pathways. We illustrate the utility of this system by targeting and deleting FADD, Caspase-8, and RIPK1. This approach can be easily adapted to any intracellular target protein, offering a robust platform for gene function analysis in mammalian cells. - Source: PubMed
Publication date: 2026/03/09
Radoua AbdelmnimAlrustom BacharWang JiaJiaBordessoules MorganeChluba JohannaPlenchette StéphanieMicheau Olivier - Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment and neuronal loss. Aberrant activation of receptor-interacting protein kinase 1 (RIPK1) plays a critical role in neuroinflammation and programmed neuronal death, making it an attractive therapeutic target. In this computational study, 16 isoxazolidine derivatives (1-16) were evaluated alongside seven reference inhibitors to identify potential RIPK1 blockers. Molecular docking analyses revealed that compound 7 exhibited the highest binding affinity toward RIPK1 (PDB ID: 7XMK), with a binding energy of -9.0 kcal mol, outperforming established inhibitors and demonstrating broad activity against AD-related targets. Density functional theory calculations showed a HOMO-LUMO energy gap of 5.209 eV, indicating favorable electronic stability. Compound 7 complied with Lipinski's rule of five and Veber's criteria and displayed excellent predictive ADMET properties, including high human intestinal absorption (HIA = 1.0), strong blood-brain barrier permeability (BBB = 0.991), and low predicted toxicity. Molecular dynamics (MD) simulations conducted over 100 ns at temperatures ranging from 300 to 320 K confirmed the stability of the RIPK1-compound 7 complex. The root-mean-square deviation (RMSD) values ranged from 5.2 to 14.0 Å (0.52-1.40 nm), indicating acceptable structural fluctuations throughout the simulation. Additionally, the radius of gyration (Rg) ranged from 2.8 to 3.8 nm, indicating that the complex maintained a relatively stable, compact conformation throughout the simulation. Principal component analysis further supported these findings, yielding cosine similarity values of 0.86-0.95. Collectively, these results highlight compound 7 as a promising RIPK1 inhibitor with favorable pharmacokinetic, electronic, and dynamic properties, underscoring its potential as a therapeutic candidate for AD. - Source: PubMed
Shila Shamima RahmanAlmatarneh Mansour HSuha Humaera NoorHossain IstiakAbdalla SaharBari Md Ahsan UlPoirier Raymond AUddin Kabir M