SLC30A3 antibody
- Known as:
- SLC30A3 (anti-)
- Catalog number:
- orb1073
- Product Quantity:
- 200 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- SLC30A3 antibody
Related genes to: SLC30A3 antibody
- Gene:
- SLC30A3 NIH gene
- Name:
- solute carrier family 30 member 3
- Previous symbol:
- ZNT3
- Synonyms:
- -
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-12
- Date modifiied:
- 2016-02-17
Related products to: SLC30A3 antibody
Related articles to: SLC30A3 antibody
- Vesicular (synaptic) zinc is a neuromodulator that fine-tunes synaptic transmission and sensory processing across many brain areas, including the brainstem, hippocampus, amygdala, and neocortex. Throughout the central auditory system, synaptic zinc plays a crucial role in modulating neurotransmission as well as baseline and adaptive sound processing. However, the developmental changes in the protein expression levels and localization of the vesicular zinc transporter (ZnT3), which loads synaptic zinc into presynaptic vesicles, remain unknown-due in part to the lack of robust ZnT3 antibodies. To address this question, we used the recently developed and validated ZnT3-HA transgenic mouse line, in which the ZnT3 protein contains a C-terminal HA epitope tag. We performed immunohistochemical staining and confocal microscopy in the central auditory system across development to localize and quantify changes in ZnT3 expression and explore potential colocalization of ZnT3 with the vesicular glutamate and GABA transporters VGLUT1 and VGAT, respectively. We found that ZnT3 expression increased significantly between P7 and P14 in both the dorsal cochlear nucleus (DCN) and the auditory cortex (AC), reaching a stable overall expression level and layer distribution by P21. Both in the DCN and AC, ZnT3 was mainly colocalized with VGLUT1. We did not find any significant levels of ZnT3 expression in either the IC or the auditory thalamus. Together, these results highlight major developmental changes in zinc signaling that may affect synaptic transmission and plasticity, as well as normal and pathological sound processing. - Source: PubMed
Publication date: 2026/08/27
Weisbord JesseCunningham Christopher LTzounopoulos ThanosBizup Brandon T - Transcranial focused ultrasound (FUS)-mediated blood-brain barrier (BBB) modulation is a promising non-invasive therapeutic strategy for targeted brain drug delivery. However, its direct regenerative potential to actively remodel the brain microenvironment and promote adult hippocampal neurogenesis remains largely unexplored owing to elusive molecular mediators. Here, we investigated whether zinc-dependent signaling contributes to adult hippocampal neurogenic responses following FUS-mediated BBB modulation. - Source: PubMed
Publication date: 2026/08/10
Choi Bo YoungShin JaewooKong ChanhoPark Min KyuHong Dae KiChung Young-SooSuh Sang WonChang Won Seok - Macroautophagy/autophagy is a critical cellular degradation pathway essential for neuronal proteostasis and synaptic function. Its decline with aging is associated with synaptic dysfunction and reduced circuit resilience. NPY (neuropeptide Y), a highly abundant brain neuropeptide, has emerged as an important regulator of autophagy and aging-related processes. In , the NPY-family peptide sNPF modulates age-related changes in presynaptic architecture via non-cell autonomous mechanisms. Here, we examined whether autophagy and NPY interact within hypothalamic NPY AGRP neurons to regulate presynaptic organization in distant brain regions. We show that autophagy in these neurons non-cell autonomously controls hippocampal presynaptic active zone architecture and proteostasis, while maintaining NPY peptide levels. Importantly, dietary supplementation of the natural polyamine spermidine restored NPY expression in the aged hippocampus, highlighting its potential to rejuvenate neuropeptide signaling. Together, these findings reveal a pathway by which hypothalamic autophagy and NPY signaling regulate hippocampal synaptic architecture, linking metabolic state to synaptic resilience.: AGRP: agouti related neuropeptide; ARC: arcuate nucleus; ATG5: autophagy related 5; AZ: active zone; BECN1/beclin1: beclin 1, autophagy related; brp: bruchpilot; BSN: bassoon; CA3-CA1: cornu ammonis 3-cornu ammonis 1; CACNA1A/CaV2.1: calcium channel, voltage-dependent, P/Q type, alpha 1A subunit; cKO: conditional knockout; gSTED: time-gated Stimulated Emission Depletion; HOMER1: homer scaffolding protein 1; KO: knockout; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MB: mushroom body; MF-CA3: mossy fiber-cornus ammonis 3; NPY: neuropeptide Y; NPY1R: neuropeptide Y receptor Y1; NPY2R: neuropeptide Y receptor Y2; NPY5R: neuropeptide Y receptor Y5; PreScale: presynaptic upscaling; RIMBP2: RIMS binding protein 2; SQSTM1/p62: sequestosome 1; sNPF: short neuropeptide F precursor; SLC30A3/ZNT3: solute carrier family 30 (zinc transporter), member 3; Spd: spermidine; Spd-S: spermidine supplementation; WT: wild-type. - Source: PubMed
Publication date: 2026/08/30
Cazzolla GiovannaToppe DavidKrause GinaKochlamazashvili GagaLützkendorf JanineSchedina Ina MStephanowitz HeikeReisenbichler Anna MariaChen XingxiangKerkhoff YannicReifenstein EricErnst Helen Mvon Kleist MaxZimmermann AndreasEisenberg TobiasMadeo FrankLiu FanHerzog HerbertAlbrecht AnneSchmitz DietmarHaucke VolkerSigrist Stephan JMaglione Marta - Microglia exhibit phenotypic plasticity between anti-inflammatory M2 and pro-inflammatory M1 states, and the transition from M2 to M1 is implicated in the progression of acute brain injuries. However, the molecular mechanisms that regulate this phenotypic shift remain poorly understood. Zn, stored in presynaptic vesicles, is extracellularly released during pathological events, such as cerebral ischemia, and modulates microglial function. In this study, we aimed to investigate the role of extracellular Zn in the M2-to-M1 transition using BV2 microglial cells. Pretreatment with ZnCl during M2 polarization significantly suppressed lipopolysaccharide-induced production of interleukin (IL)-6 and tumor necrosis factor-α following the phenotypic shift. Among the zinc transporters, Zrt- and Irt-related protein 12 (ZIP12) expression was markedly upregulated by IL-4 stimulation, and siRNA-mediated knockdown of ZIP12 abolished the Zn-mediated suppression of pro-inflammatory cytokine production. Furthermore, ZIP12 knockdown reduced intracellular Zn accumulation in IL-4-treated microglia, as revealed by FluoZin-3 fluorescence. These findings indicate that extracellular Zn is taken up via ZIP12 during M2 polarization and subsequently acts to suppress pro-inflammatory cytokine production, thereby restraining the shift toward an M1 phenotype. - Source: PubMed
Publication date: 2025/10/30
Aratake TakaakiHigashi YouichirouShimizu TakahiroFukata SatoshiSaito Motoaki - Alzheimer's disease (AD) is a progressive neurodegenerative disorder with unclear pathogenic mechanisms. Dysregulated zinc metabolism contributes to AD pathology. This study aimed to identify zinc metabolism-related hub genes to provide potential biomarkers and therapeutic targets for AD. - Source: PubMed
Publication date: 2025/11/13
Bai RuyuCheng ZhiyunDiao Yong