SLP-2 Antibody
- Known as:
- SLP-2 Antibody
- Catalog number:
- XW-8029
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SLP-2 Antibody
Related genes to: SLP-2 Antibody
- Gene:
- KLF16 NIH gene
- Name:
- Kruppel like factor 16
- Previous symbol:
- -
- Synonyms:
- NSLP2, BTEB4, DRRF
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-27
- Date modifiied:
- 2016-06-03
- Gene:
- RN7SL5P NIH gene
- Name:
- RNA, 7SL, cytoplasmic 5, pseudogene
- Previous symbol:
- RN7SLP2, RN7SL249P
- Synonyms:
- 7LEM1
- Chromosome:
- 9p23
- Locus Type:
- pseudogene
- Date approved:
- 1994-07-14
- Date modifiied:
- 2014-11-19
- Gene:
- SYTL2 NIH gene
- Name:
- synaptotagmin like 2
- Previous symbol:
- -
- Synonyms:
- FLJ20163, FLJ21219, KIAA1597, exophilin-4, CHR11SYT, SLP2, SGA72M, MGC102768, PPP1R151
- Chromosome:
- 11q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-25
- Date modifiied:
- 2015-11-18
Related products to: SLP-2 Antibody
Related articles to: SLP-2 Antibody
- Osteoarthritis (OA) is associated with chondrocyte dysfunction and cartilage degeneration, but how mitochondrial homeostasis is maintained during OA progression remains incompletely understood. Here, we show that Stomatin-like protein 2 (STOML2) is downregulated in IL-1β-stimulated chondrocytes and in human OA cartilage. STOML2 depletion impairs oxidative phosphorylation, elevates mitochondrial reactive oxygen species, and promotes chondrocyte senescence and ferroptotic cell death. Mechanistically, STOML2 interacts with the mitochondrial Na/Ca exchanger (NCLX) to support mitochondrial Ca efflux and metabolic stability. Restoring STOML2 enhances NCLX-dependent Ca handling, mitigates mitochondrial Ca overload and the glycolytic shift, and improves ATP production. In a rat OA model, intra-articular delivery of STOML2 attenuates cartilage degeneration and reduces inflammatory changes in the joint. Together, these findings identify a STOML2-NCLX axis that safeguards mitochondrial Ca homeostasis and chondrocyte viability, suggesting STOML2 as a potential therapeutic target for OA. - Source: PubMed
Xie FeiMiao KunWu HaoWu Xuejun - The innate immune cGAS-STING pathway is activated by cytosolic double-stranded DNA (dsDNA) to induce type I interferon (IFN) response, which is essential for mounting the antiviral response. However, STING activation during viral infection is often insufficient to achieve complete viral clearance, suggesting the existence of additional mechanisms that evade its activity. Here, we identified COX2/PGE as a negative regulator of STING activation, particularly in response to arising cytosolic mitochondrial DNA (mtDNA) generated during HSV-1 infection. Mechanistically, PGE , through the EP4-cAMP-PKA axis, induces mitophagy to remove defective mitochondria and hence prevent the accumulation of immunostimulatory cytosolic mtDNA, thereby dampening STING-mediated type I IFN and antiviral response. Furthermore, we identified STOML2 as a downstream target of PKA that connects mitochondrial quality control with the regulation of innate immune signaling. Together, our findings establish the COX2/PGE /PKA axis as a negative regulator of mtDNA-STING signaling that may be targeted to potentiate STING-mediated type I IFN and innate immunity. - Source: PubMed
Publication date: 2026/04/06
Vo Pham Thuy TienCicero JulienWang ZichenHakozaki HiroyukiHoang Thomas SRafael Adame-Garcia SendiRamms Dana JSato KuniakiStevenson EricaZhou YuanFan KatieSwaney Danielle LKrogan Nevan JSchöneberg JohannesManor UriGutkind J Silvio - - Source: PubMed
Publication date: 2026/03/27
Cheng TingtingZhao XinRuan Yuelu - Earlier research observed the effects of plasma proteins on ischemic stroke (IS). This Mendelian randomization (MR), in vivo study additionally assesses the associations of localized populations of plasma proteins with IS to further confirm the causality and explore drug targets. - Source: PubMed
Publication date: 2026/03/17
Ren HaoxuDing YingyueWang RuonanLi JinjianYang ChenganWang XuZhao Dexi - Understanding susceptibility factors of sepsis is crucial for early diagnosis and development of personalized treatment strategies. However, the genetic determinants for initiation and progression of sepsis remain unclear. Here, we showed that the expression levels of estrogen receptor (ER) β are significantly reduced in the peripheral blood of sepsis patients, which were negatively correlated with disease severity. The results from human samples and experimental animals demonstrated that ERβ deficiency enhances the body's susceptibility to sepsis by inducing macrophage pyroptosis, thereby impairing bacterial clearance. Mechanistically, ERβ deficiency enhanced fatty acid oxidation, increased acetyl-CoA levels, and promoted acetylation of stomatin-like protein 2 (Stoml2) at K221, leading to mitochondrial dysfunction and macrophage pyroptosis. Mutating the Stoml2 K221 site mitigated these effects and improved survival of septic mice. These findings suggest ERβ deficiency as a potential genetic factor in sepsis susceptibility. - Source: PubMed
Publication date: 2026/03/17
Zhu YanrongLi GangGuo YileiHe YueZhang WanyiGao LeiZhang JingGuo PengxiangLin HaochangZhang WenjieWei ZhifengXia YufengDai Yue