STAT3
- Known as:
- STAT3
- Catalog number:
- RP17131630005
- Product Quantity:
- 5 µg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- STAT3
Related genes to: STAT3
- Gene:
- STAT3 NIH gene
- Name:
- signal transducer and activator of transcription 3
- Previous symbol:
- -
- Synonyms:
- APRF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT3
Acpin1,Acrosomal protein ACPIN1,Mouse,Mus musculus,Sipar,STAT3-interacting protein as a repressorAnserine Signal Transducer And Activator Of Transcription 3 Elisa Kit (STAT3)Anserine anti - Signal Transducer And Activator Of Transcription 3 Elisa Kit (STAT3)Anti- STAT3 (Ab-705) AntibodyAnti- STAT3 (Ab-705) AntibodyAnti- STAT3 (Ab-727) AntibodyAnti- STAT3 (Ab-727) AntibodyAnti- STAT3 (Phospho-Ser727) AntibodyAnti- STAT3 (Phospho-Ser727) AntibodyAnti- STAT3 (Phospho-Tyr705) AntibodyAnti- STAT3 (Phospho-Tyr705) AntibodyAnti-Human STAT3, Rabbit PolyclonalAnti-Human STAT3, Rabbit Polyclonal affinity purified IgGanti-n STAT3 , Rabbit polyclonal to n STAT3 , Isotype IgG, Host RabbitAnti-phospho-STAT3 (pTyr705<_SUP>) produced in rabbit Antibody Related articles to: STAT3
- Exposure to agricultural organic dust increases the risk of respiratory diseases. Aryl hydrocarbon receptor (AhR), a transcription factor activated by environmental chemicals and endogenous metabolites, regulates immune and inflammatory responses, but its role in organic dust-induced lung inflammation is not known. Our study elucidated mechanisms by which AhR modulates bronchial epithelial cell inflammatory responses induced by poultry farm organic dust extract (DE) and organic dust-associated (OD) bacterial extracellular vesicles (EVs). - Source: PubMed
Publication date: 2026/09/10
Meganathan VelmuruganKusampudi ShilpaStenhouse MaxineBoggaram Vijay - Myeloproliferative neoplasms (MPN) are driven by the oncoproteins JAK2V617F, mutant calreticulin (CALR), and mutant thrombopoietin receptor (TPOR; MPL), all of which activate JAK/STAT signaling. While JAK2 signaling is engaged in all MPNs, TYK2 is dispensable for JAK2V617F-driven disease. Here, we hypothesized a distinct role for TYK2 in CALR-mutant driven MPN. We found constitutive TYK2 phosphorylation in CALRdel52/ins5- and MPLW515K- but not JAK2V617F-expressing cells. Structural modeling predicted similar TPOR-binding affinities for JAK2 and TYK2, while micropatterning experiments demonstrated that both JAK2WT and JAK2V617F displace TYK2 from the receptor. The TYK2 inhibitor deucravacitinib reduced viability and STAT3/5 phosphorylation in CALRdel52/ins5- and MPLW515K- but not JAK2V617F-mutant cells, with enhanced efficacy when combined with the JAK2-selective inhibitor fedratinib. Cellular response correlated with JAK2 protein abundance, as CALRins5 JAK2 clones outcompeted JAK2 clones upon TYK2 inhibition. In primary samples, deucravacitinib significantly suppressed colony growth in ET and PMF but not PV, and selectively reduced CALR- but not JAK2V617F-mutant allele burden. Similarly, CALR-mutant patient-specific iPSC-derived CD34 progenitors showed increased TYK2 phosphorylation and were more sensitive to TYK2 inhibition than their JAK2V617F counterparts. These findings identify TYK2 as a selective vulnerability in CALR-mutant MPN and support combined TYK2/JAK2 inhibition strategies to overcome JAK2-dependent resistance. - Source: PubMed
Publication date: 2026/09/24
Kalmer MilenaWirths ChiaraLemanzyk RebeccaPiergentili AlessiaMönnig MiaZhou ChunxiaoJunge BärbelGoßen JonasGupta SiddharthSchulz LauraSpitzer AnnaTillmann StefanKricheldorf KimSchifflers JoellePannen KristinaGalauner AngelaPiehler JacobPecquet Christiande Toledo Marcelo A SConstantinescu Stefan NRossetti GiuliaKoschmieder SteffenChatain Nicolas - Metastatic pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest solid cancers, portending poor patient outcomes due to challenges in precise diagnosis and therapeutic resistance. Extensive molecular heterogeneity of metastatic tumours and their frequent evasion from clinical detection represent critical bottlenecks in disease management. Despite substantial research efforts, optimal clinical management remains an ongoing challenge. In this review, we outline the current understanding of metastatic pancreatic cancer, including its clinical features in patients. Emerging evidence highlights the pivotal roles of dynamic interactions between cancer cells and organ-specific and niche-specific microenvironments during metastatic spread. We further summarise the known molecular characteristics of metastatic PDAC and the preclinical models developed in pancreatic cancer research for functional interrogation. Finally, based on the current knowledge of this disease, we discuss existing limitations and future opportunities for advancing precision oncology approaches. These efforts may open promising avenues for the development of more effective clinical strategies aimed at mitigating metastasis in PDAC. - Source: PubMed
Publication date: 2026/09/24
Min JiminLiaki VasilikiYu Peter YGuerra CarmenMaitra Anirban - Astrocytes play a crucial role in controlling homeostasis of the central nervous system (CNS), synapse, metabolism and neuroimmune communications. The growing body of evidence indicates that astrocyte dysfunction plays the leading role in the pathogenesis of Alzheimer's disease (AD). Reactive astrogliosis, characterised by cell hypertrophy, transcriptional reprogramming, and elevated glial fibrillary acidic protein (GFAP) expression, arises early in response to amyloid-β accumulation, neuroinflammation, and blood-brain barrier (BBB) disruption. Transcriptional, epigenetic and inflammatory signalling, including JAK/STAT3, NF-KB, MAPK and non-coding RNAs, control the expression of GFAP, which is a structural intermediate filament protein. High GFAP shows activation of astrocytes and a part of disrupted neuronal support, glutamate imbalance, oxidative distress and defective glymphatic clearance. Consequently, GFAP is an efficient biomarker in CSF, plasma, and saliva, which is associated with amyloid pathology, cognitive impairment, and AD. The knowledge of the astrocyte responses to GFAP can be used to extract significant information about AD mechanisms and find opportunities to identify diagnosis, prognosis and therapy. - Source: PubMed
Publication date: 2026/02/07
Upadhyay RiddhiSrinivasan Thanga BalajiUmapriya RChandrapragasam VaniSevanan Murugan - Mammary gland involution is a tightly coordinated post-lactational remodeling program that restores tissue homeostasis and preserves the capacity of the gland for subsequent lactation. Although this process requires extensive epithelial regression, stromal remodeling, and immune cell recruitment, the mechanisms that prevent premature or excessive involution remain incompletely understood. Here, we examined the role of metastasis-associated protein 1 (MTA1) in regulating mammary gland involution. - Source: PubMed
Publication date: 2026/09/24
Kim Seung-SuLee Sang-HeonJeong CheolheeKwon Hae-MinHwang SewonLim Ga YoungKa Na-LeeLee Mi-Ock