DUSP11 Antibody
- Known as:
- DUSP11 Antibody
- Catalog number:
- XW-7841
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- DUSP11 Antibody
Related genes to: DUSP11 Antibody
- Gene:
- DUSP11 NIH gene
- Name:
- dual specificity phosphatase 11
- Previous symbol:
- -
- Synonyms:
- PIR1
- Chromosome:
- 2p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-06
- Date modifiied:
- 2015-11-05
Related products to: DUSP11 Antibody
Related articles to: DUSP11 Antibody
- Multiple members (DUSP1-29) of dual-specificity phosphatase (DSP) family are key regulators of mitogen-activated protein kinases (MAPKs), which regulate numerous physiological responses. Eight DUSPs are also named MAPK phosphatases (MKPs). DUSP dysregulation contributes to the pathogenesis of various human inflammatory and chronic diseases. Downregulation of DUSP1, DUSP3, DUSP11, and DUSP22, as well as upregulation of DUSP4, DUSP6, and DUSP23 are involved in human autoimmune diseases. Besides autoimmune diseases, reduction of DUSP1, DUSP2, and DUSP14, as well as induction of DUSP8 contribute to the pathogenesis of allergic diseases. Additionally, decreased levels of DUSP2, DUSP11, DUSP22, and DUSP28 are associated with human inflammatory bowel diseases. Moreover, deficiency of 10 DUSPs, as well as induction of DUSP4 are associated with metabolic diseases. Downregulation of 5 DUSPs are involved in cardiovascular disease pathogenesis; in contrast, upregulation of other 5 DUSPs are correlated with cardiovascular diseases. Collectively, dysregulated DUSPs could be diagnostic biomarkers and therapeutic targets for inflammatory diseases. Due to complex expression patterns of DUSPs, it is crucial to study the regulatory mechanisms of individual DUSPs in various inflammatory and chronic diseases. In this review, we summarize the roles and regulatory mechanisms of DUSPs in human inflammatory and chronic diseases. We also discuss the potential therapeutic applications of DUSP agonists/inhibitors in human inflammatory and chronic diseases. - Source: PubMed
Publication date: 2026/05/06
Wang Chia-WenChuang Huai-ChiaTan Tse-Hua - The CRISPR-Cas13 system enables programmable RNA targeting with potential applications in therapeutics and research. However, while PspCas13b mediates efficient RNA knockdown following transient transfection, stable lentiviral delivery results in minimal activity, limiting its utility. Here, we performed a genome-wide CRISPR-Cas9 knockout screen to identify mammalian factors that restrict PspCas13b activity. We discovered that DUSP11, an RNA triphosphatase, suppresses PspCas13b function by dephosphorylating the 5'-triphosphate of Pol III-transcribed guide RNAs (gRNAs), triggering their degradation. DUSP11 knockout increased gRNA levels 2.5-4-fold and enhanced PspCas13b-mediated knockdown across multiple cell lines. This enhancement was sustained for at least 27 days and enabled targeting of endogenous transcripts previously refractory to PspCas13b. Our findings reveal an unexpected host restriction of bacterial CRISPR systems and demonstrate that gRNA levels are a limiting factor. We provide a simple strategy to improve PspCas13b activity in mammalian cells. These results have implications for developing PspCas13b-based therapeutics and suggest that systematic identification of host factors regulating CRISPR components could enhance genome editing technologies. - Source: PubMed
Purcell JacobLiu LingCalvert Roland WHayes Brooke KHuang ChengDavidovich ChenKnott Gavin JRosenbluh Joseph - The discovery of immune checkpoints and the rapid growth of immuno-oncology have sparked efforts to utilize the immune system to treat a wide range of cancer types/subtypes. Although the major focus of immuno-oncology over the past decades has been to manipulate the adaptive immune system, recent attention has been given to manipulating the innate immune system to treat cancer and/or to enhance adaptive responses. In this study, we detailed the intracellular protein dual specificity phosphatase 11 (DUSP11) as an innate immune checkpoint in non-small cell lung cancer adenocarcinoma (LUAD). The expression of this atypical phosphatase was correlated with patient survival for multiple cancer types, and we reported here that its activity was important for the viability of lung cancer cells in vitro. Specifically, we demonstrated that DUSP11 knockdown in LUAD cells induces apoptosis and an innate immune response capable of activating other cells in vitro, and we provided evidence that these phenotypes are primarily mediated by the pattern recognition receptor, retinoic acid-inducible gene I. Finally, we showed that the expression of DUSP11 was important for tumor engraftment and growth of human LUAD in mice. Overall, these data are the first to establish DUSP11 as an immunosuppressive, pro-neoplastic, and potentially targetable protein in LUAD. In addition, our data suggest that the anticancer mechanisms induced by diminishing the activity of DUSP11 are likely to be generalizable to other cancer types such as breast and skin cancers, warranting future investigation and highlighting therapeutic potential. - Source: PubMed
Thomas Brian JBai XueCryer Benjamin JEscobar Sydney MAllen Lee-Ann HDaniels Mark ALange Margaret JBurke Donald H - Proper recognition of viral pathogens is an essential part of the innate immune response. A common viral replicative intermediate and chemical signal that cells use to identify pathogens is the presence of a triphosphorylated 5' end (5'ppp) RNA, which activates the cytosolic RNA sensor RIG-I and initiates downstream antiviral signaling. While 5'pppRNA generated by viral RNA-dependent RNA polymerases (RdRps) can be a potent activator of the immune response, endogenous RNA polymerase III (RNAPIII) transcripts can retain the 5'ppp generated during transcription and induce a RIG-I-mediated immune response. We have previously shown that host RNA triphosphatase dual-specificity phosphatase 11 (DUSP11) can act on both host and viral RNAs, altering their levels and reducing their ability to induce RIG-I activation. Our previous work explored how experimentally altered DUSP11 activity can impact immune activation, prompting further exploration into natural contexts of altered DUSP11 activity. Here, we have identified viral DUSP11 homologs (vDUSP11s) present in some avipoxviruses. Consistent with the known functions of host DUSP11, we have shown that expression of vDUSP11s: 1) reduces levels of endogenous RNAPIII transcripts, 2) reduces a cell's sensitivity to 5'pppRNA-mediated immune activation, and 3) restores virus infection defects seen in the absence of DUSP11. Our results identify a context where DUSP11 activity has been co-opted by viruses to alter RNA metabolism and influence the outcome of infection. - Source: PubMed
Publication date: 2025/04/21
Szymanik Kayla HRex Emily APothireddy Vamshikrishna RGammon Don BHancks Dustin CSullivan Christopher S - Schisandrin B (Sch B) is an active component in Schisandra chinensis exerting anti-cancer effect, but the mechanism is obscure. This study was designed to explore the mechanism of Sch B against colorectal cancer (CRC). - Source: PubMed
Publication date: 2025/03/15
Sun JianguoWang ZhipengYun YunleiFeng YingqiLiu ZhijunCui LiliTang MaoYe LiyaLiang ZhengyanChen WanshengGao Shouhong