ACCS
- Known as:
- ACCS
- Catalog number:
- 000999A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACCS
Related genes to: ACCS
- Gene:
- ACCS NIH gene
- Name:
- 1-aminocyclopropane-1-carboxylate synthase homolog (inactive)
- Previous symbol:
- -
- Synonyms:
- PHACS, ACS
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-01-25
- Date modifiied:
- 2018-06-26
Related products to: ACCS
Related articles to: ACCS
- A search for studies was conducted through PubMed, Embase, Scopus, Web of Science, Lilacs, Cochrane, CINAHL (EBSCOhost), and gray literature (Google Scholar), using established screening criteria. The risk of bias was assessed for all articles. Meta-analysis was performed using Review Manager v. 5.3. - Source: PubMed
Publication date: 2026/09/26
da Silva Weslay Rodriguesda Silva Cavalcanti Jonathan FrançaLima Júlia Vanessa Bezerrada Silva Barros Caio Césarda Silva Leorik PereiraSobral Ana Paula Veras - Postnatal mouse retinal development is a multi-faceted process involving the coordinated interaction of spontaneous neural activity as retinal waves, vascular plexus growth, and programmed cell death. While these processes are known to interact at a coarse scale, the specific mechanisms integrating them have remained elusive. Using large-scale, wide-field calcium imaging, high-density multielectrode array recordings, single-cell RNA sequencing, and immunohistochemistry, we characterise a tightly aligned centrifugal expansion pattern during retinal development. This pattern is common to stage II retinal wave onsets, vascular development, Heme oxygenase-1 (Hmox1) expressing microglia, apoptotic cell markers, and a novel set of auto-fluorescent cluster complexes (ACCs) identified in this study. Apoptotic cells are known to upregulate functional pannexin-1 (PANX-1) hemichannels. These voltage-gated channels release purinergic molecules which act as 'eat me' signals to neighbouring microglia. PANX-1 hemichannel blockade with the drug probenecid results in a profound decrease in spontaneous wave frequency and strength, suggesting that retinal waves are indeed triggered by these apoptotic cells. Taken together, our observations suggest that spontaneous waves are initially triggered in hotspots by hyperactive apoptotic retinal ganglion cells (RGCs) in unvascularised retinal areas. These apoptotic cells release purinergic molecules via PANX-1 hemichannels, leading to wave generation. This hyperactivity leads to local hypoxic conditions, which, coupled with high extracellular ATP concentrations, promotes angiogenesis. Once blood vessels reach a particular hotspot, ATP release activates Hmox1-positive microglia, which engulf the dying RGCs, creating the auto-fluorescent clusters. Herein, we present a unified mechanism linking causally linking early neural activity, programmed cell death, and angiogenesis in the mammalian retina. - Source: PubMed
Publication date: 2026/09/24
Savage Michael ABertram Coride Montigny JeanThorne Courtney AQueen RachelLako MajlindaHilgen GerritSernagor Evelyne - We study the emergence of a unique dynamical state, termed the asymmetric coherent cluster (ACC), in ring networks of identical Stuart-Landau oscillators arising from the interplay of symmetric and asymmetric couplings. The ACC state constitutes an intermediate regime between the splay (SP) and complete synchronization (CS) states, exhibiting macroscopic coherence despite persistent microscopic phase drift of the coupled oscillators. Remarkably, in the ACC state, oscillators self-organize into a stationary, symmetry-broken macroscopic structure while remaining dynamically nonstationary at the microscopic level. The transition from the SP state to the ACC state occurs via an abrupt frequency-unlocking process and is mediated by the breakdown of a stable limit cycle into an invariant torus. In contrast, the ACC-CS transition proceeds through gradual frequency locking accompanied by a continuous increase in global coherence. In this regime, the invariant torus collapses smoothly onto a fully synchronized limit cycle via a reverse supercritical Neimark-Sacker bifurcation. Numerical simulations support the theoretical analysis and demonstrate the robustness of the ACC state. These results demonstrate how competing symmetric and asymmetric interactions give rise to nontrivial collective dynamics, offering a route to coherent macroscopic states beyond conventional phase-locked synchronization. Furthermore, the robustness of ACCs and their existence over a broad range of coupling parameters strongly suggest their experimental realizability. - Source: PubMed
Mendola Naveen KumarPrasad AwadheshSingh Thounaojam Umeshkanta - Anxiety is an adaptive response essential for survival that integrates external stimuli, internal states, memory, and decision making to respond to perceived threats. When dysregulated, it can become excessive and persistent, contributing to psychiatric and neurological disorders. The anterior cingulate cortex (ACC) integrates cognitive, emotional, interoceptive, and autonomic information and serves as a key hub in anxiety-related circuits. However, its subregion- and pathway-specific roles remain incompletely integrated across species. This review examines the cytoarchitectural and cellular organization of ACC subregions and their proposed correspondence in humans, non-human primates, and rodents. We then review ACC connectivity with the amygdala, hippocampus, insula, and bed nucleus of the stria terminalis and propose an integrative model in which ACC effects depend on subregion, projection target, and behavioral context. We also summarize structural, functional, connectivity, and neurochemical alterations of the ACC in anxiety-related disorders and neurodegenerative diseases with prominent anxiety symptoms. Finally, we discuss the strengths and limitations of rodent and non-human-primate models and identify priorities for future mechanistic and translational studies. Together, this review provides a timely and comprehensive view of the ACC's role in adaptive and pathological anxiety and offers a framework for advancing mechanistic and translational research. - Source: PubMed
Publication date: 2026/08/26
Dew EmilyJones AlexisSaggu ShaliniPozzo-Miller LucasWang Qin - Mitotane is e first-line medical treatment for adrenocortical carcinoma (ACC). Mitotane has substantial dr awbacks, including severe toxicity and contralateral gland destruction, whilst effective in only 25-30% of ACCs. To improve patient selection for mitotane therapy, this study aimed to identify tissue biomarkers associated with in vitro mitotane response. - Source: PubMed
Publication date: 2026/09/09
Vietor Charlotte LIyer Anand Mvan Koetsveld Peter MSwagemakers Sigrid M Avan der Spek Peter JBindels Eric M JZeneyedpour LonaLuider Theo Mvan Velthuysen Marie-Louise FAssié GuillaumeJouinot AnneHofland Johannesde Herder Wouter WVerhoef Cornelisvan Ginhoven Tessa MFeelders Richard AHofland Leo J