Ask about this productRelated genes to: RIPK1 antibody
- Gene:
- RIPK1 NIH gene
- Name:
- receptor interacting serine/threonine kinase 1
- Previous symbol:
- -
- Synonyms:
- RIP
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2015-11-17
Related products to: RIPK1 antibody
Related articles to: RIPK1 antibody
- Epithelial to mesenchymal transition (EMT) is a process of trans-differentiation important for development, inflammation and cancer. Transforming Growth Factor-β (TGFβ) is a physiologically relevant inducer of EMT. We had recently characterized the adenosine analogue, adenosine kinase inhibitor 5-Iodotubercidin (5-ITu), as a compound which preferentially sensitizes MK2-deficient cells to TNFα-induced, RIPK1-dependent cell death. Here we investigated the effect of 5-ITu on TGFβ-induced EMT. 5-ITu suppressed TGFβ-induced morphological changes and migration in A549 (lung cancer) and PANC1 (pancreatic cancer) cell lines. Consistent with these effects, there was significant suppression of EMT markers as indicated by qPCR, immunoblotting and immunofluorescence and confocal microscopy. Mechanistic investigations revealed that 5-ITu-mediated EMT suppression was independent of adenosine kinase inhibition and RIPK1 activation. 5-ITu suppressed NFκB activity in cells undergoing EMT and IKK inhibition phenocopied the effect of 5-ITu on EMT. The effect of 5-ITu on EMT was lost upon IκBα knockdown. Kinase assays revealed IKKβ as a potential direct target of 5-ITu. We identified a TGFβ-associated, NFκB-dependent gene signature consisting of 4 genes, that are differentially regulated upon 5-ITu treatment. Interestingly, this 4 gene signature could predict survival in lung and pancreatic cancer. The identification of this role for the multitarget kinase inhibitor 5-ITu in NFκB activity-dependent EMT, in addition to RIPK1-dependent necroptosis has potential implications in anticancer strategies. - Source: PubMed
Publication date: 2026/09/11
Bhattacharya SayariManjari MuskanGanesh VaishnaviMenon Manoj BDhamija Sonam - RIPK1, a protein regulating inflammatory signalling and cell death, is implicated in amyotrophic lateral sclerosis (ALS) pathophysiology. SAR443820 is a selective, oral, CNS-penetrant, reversible RIPK1 inhibitor. We aimed to evaluate the safety, tolerability, and efficacy of SAR443820 in participants with ALS. - Source: PubMed
Cudkowicz Merit EShefner Jeremyvan den Berg Leonard HChio AdrianoFan DongshengGroßkreutz JulianLunetta ChristianTsai Richard MLi YeWallstroem ErikXiong LiChen YixinAtassi Nazem - PANoptosis is an integrated inflammatory form of programmed cell death mediated by the PANoptosome, which coordinates the core molecular networks of pyroptosis, apoptosis, and necroptosis. In recent years, PANoptosis-related signaling has been implicated in a wide range of renal pathological processes, including sepsis-associated acute kidney injury, ischemia-reperfusion injury, drug- or toxin-induced nephropathy, diabetic nephropathy, chronic kidney disease, renal fibrosis, and clear cell renal cell carcinoma. Mechanistically, these processes may involve the coordinated activation of key molecules, including ZBP1, AIM2, RIG-I, RIPK1, CASP8, NLRP3, GSDMD/GSDME, and RIPK3/MLKL. However, most existing studies remain largely confined to marker co-expression, animal models, or bioinformatics-based analyses, while direct evidence of PANoptosome assembly and functional dependence remains limited. Notably, the predominant cell types, upstream stimuli, and biological consequences of PANoptosis vary substantially across disease contexts. In non-neoplastic kidney diseases, PANoptosis is commonly associated with inflammatory injury and fibrotic progression; in contrast, in clear cell renal cell carcinoma, PANoptosis-related molecular signatures are more frequently linked to prognostic stratification and prediction of immunotherapy response. Future studies should place greater emphasis on validating PANoptosome assembly, defining cell lineage-specific localization, establishing temporal causality, and confirming findings in clinical samples. Integrating single-cell multi-omics, spatial transcriptomics, and functional intervention models will help advance PANoptosis from a mechanistic concept toward precise kidney disease subtyping and network-based targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/08/25
Yang ShifanLi XunZhang ChenmingMa SichengZhou Yingda - Alopecia areata is a non-scarring autoimmune disease that is usually characterized by patchy or diffuse hair loss. The collapse of the immunological privilege of hair follicles and activation of cytotoxic T-cell pathways, regulated by metabolic, psychological, and environmental variables, cause this disorder. Advances in the fields of immunology and regenerative medicine have identified new therapeutic targets and novel approaches. - Source: PubMed
Publication date: 2026/08/28
Thakur RitikaGill ParinaBala RajniSaraswat RishiKaur Ramandeep - Mycobacterium tuberculosis (M. tuberculosis) has evolved to survive within host phagocytes while provoking inflammatory tissue destruction, a delicate balance that is critically shaped by programmed cell death (PCD). Rather than acting as isolated linear pathways, apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy/xenophagy, ETosis/NETosis, PARP1-AIF/parthanatos-related signaling, and PANoptosis-related signaling form an interconnected network that determines macrophage fate, granuloma integrity, bacterial dissemination, and immunopathology. In this Review, we discuss how M. tuberculosis and host-derived signals engage canonical cell-death modules, including caspases, RIPK1/RIPK3-MLKL, inflammasomes-gasdermins, ROS-iron-lipid peroxidation circuits, PARP1-AIF signaling, and autophagy machinery. We highlight context-dependent effects whereby apoptosis and autophagy may promote bacterial containment, whereas necrotic and inflammatory forms of death can either enhance antimicrobial immunity or drive caseation and tissue damage. We further evaluate emerging evidence for crosstalk among PCD modalities, with particular attention to shared molecular checkpoints and the still-evolving concept of PANoptosis in tuberculosis. Finally, we discuss host-directed therapeutic strategies aimed at recalibrating, rather than simply blocking or activating, cell-death pathways. A network-based understanding of PCD in M. tuberculosis infection provides a crucial framework for developing adjunctive therapies that enhance pathogen control while limiting destructive inflammation. Unlike pathway-centered summaries, this Review reframes M. tuberculosis-induced cell death as a dynamic network in which shared molecular hubs, compensatory switching, and lesion-stage-specific microenvironments jointly determine disease outcome. - Source: PubMed
Publication date: 2026/09/07
Zhang QingChang De