Ask about this productRelated genes to: CEND1 Blocking Peptide
- Gene:
- CEND1 NIH gene
- Name:
- cell cycle exit and neuronal differentiation 1
- Previous symbol:
- -
- Synonyms:
- FLJ90066, BM88
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2006-06-14
- Date modifiied:
- 2014-11-19
Related products to: CEND1 Blocking Peptide
Related articles to: CEND1 Blocking Peptide
- Parkinson's disease (PD) is a chronic neurodegenerative disorder featuring dopaminergic neuron loss, which is associated with mitochondrial dysfunction. Astragalus polysaccharide (APS) extracted from possesses antioxidant, anti-inflammatory, and neuroprotective properties. APS was previously revealed to exert neuroprotective effects in experimental PD models. However, the underlying mechanism remains poorly understood. Therefore, our study was designed to reveal the molecular mechanism through which APS exerts neuroprotective effects in PD. - Source: PubMed
Publication date: 2026/01/15
Cong ZeweiLi ChanSun MengqinYu YanZhang Xianmei - Mitochondrial dysfunction is a critical contributor to neuronal damage in acute ischemic stroke (AIS), and targeting mitochondrial function represents a promising therapeutic strategy. This study unveils the pivotal role of Cend1 protein in ischemic stroke and elucidates its underlying mechanisms. Using Cend1 knockout (KO) mice, Cend1 deficiency was shown to exacerbate cerebral ischemia/reperfusion injury, as evidenced by enlarged infarct volume, worsened neurological deficits in motor coordination and grip strength, together with alterations in mitochondrial membrane potential (ΔΨm), mPTP opening, ATP content, and the activities of respiratory Complex I and V. Mechanistically, Cend1 forms dimers via conserved GXXXA motifs in its transmembrane domain to enhance ATP synthesis. Disruption of dimerization of Cend1 (such as G130P mutation) destabilized Cend1, accelerating its degradation and abolishing ATP-enhancing effects. Atp5f1b, a mitochondrial ATP synthase subunit, was found to interact with Cend1. Furthermore, screening identified the small-molecule compound Tianeptine (TNT), which stabilizes Cend1 dimers, elevates ATP levels, and confers neuroprotection in a Cend1-dependent manner. Notably, TNT's efficacy was abolished in Cend1 KO mice, highlighting its reliance on Cend1. The findings support the Cend1/Atp5f1b interaction as a potential mitochondria-targeted mechanism, offering innovative strategies to combat ischemic stroke by enhancing bioenergetic resilience. - Source: PubMed
Publication date: 2025/12/31
Li HaoYang YiZhang MengGuo EricLi ZehengWan BoMiao ZhigangGe WeiChen GangXu Xingshun - Neurons and brown adipocytes rely on rapid ATP production from accelerated glucose metabolism to sustain bursts of activity upon stimulation, a process known as activity-dependent glucose metabolism. The first committed step in this pathway, the hexokinase I (HK1)-catalyzed phosphorylation of glucose, consumes ATP, raising the question of how this reaction can be accelerated when cytosolic ATP becomes limiting during stimulation. We identify Cell Cycle Exit and Neuronal Differentiation protein 1 (CEND1), expressed in both cell types, as a critical regulator of this process. Loss of CEND1 impairs activity-dependent glucose utilization, ATP generation, and stimulation-evoked activity both and . Mechanistically, CEND1 assembles a complex with HK1, voltage-dependent anion channel 1 (VDAC1), and adenine nucleotide translocase 1 (ANT1) at hemifusion-like membrane junction between the outer/inner mitochondrial membrane, channeling mitochondrially derived ATP directly to HK1. These findings uncover a previously unrecognized mechanism that sustains activity-dependent glucose metabolism, with broad implications for energy homeostasis in specialized cell types. - Source: PubMed
Publication date: 2025/12/19
Yang DengbaoMolinaro GemmaNijem NadineZhang ChuanhaiPenny DylenBai MeijuanLin Mei-JungWen XiaodongPena SalvadorWansapura JanakaGaitanou MariaMatsas RebeccaWang BoyuanBaniasadi HamidHan YanGibson JayHuber KimberlyZeng Xing - As a transmembrane glycoprotein overexpressed in various tumors, neuropilin-1 (NRP-1) is involved in tumor progression, angiogenesis, and immune evasion. This study developed a novel PET cyclic peptide radiotracer [Ga]Ga-DOTA-CEND1 for NRP-1 detection specifically and sensitively across multiple tumor types, potentially guiding personalized NRP-1 therapeutic regimens. NRP-1 expression was assessed and confirmed through immunohistochemical analysis of tissue microarrays, Western blot, immunohistochemistry, and immunofluorescence staining. The biochemical properties of the probe were investigated through radiochemical purity, lipid-water partition coefficient, pharmacokinetics, in vivo and in vitro stabilities, and biosafety studies. To determine diagnostic sensitivity and clinical applicability, cellular uptake assays, micro positron-emission tomography/computed tomography (PET/CT), blocking studies, and ex vivo biodistribution were performed in four NRP-1 positive tumor models (fibrosarcoma, TNBC, NSCLC, and pancreatic tumor) and one NRP-1-negative model (cervical tumor). [Ga]Ga-DOTA-CEND1 demonstrated >95% radiochemical purity, optimal pharmacokinetics, favorable hydrophilicity, robust in vivo and in vitro stability, and an ideal biosafety profile. Micro PET/CT at 1 h postinjection revealed significantly higher tumor uptake in NRP-1 positive tumor models than in the NRP-1 negative tumor model, while coinjection with nonradioactive CEND-1 significantly reduced tumor uptake, and tumor-to-muscle ratios aligned with NRP-1 expression levels, confirming the specificity and sensitivity of the radiotracer. As the first PET cyclic peptide radiotracer, [Ga]Ga-DOTA-CEND1 holds great potential for noninvasively detecting NRP-1 expression across tumor types, optimizing NRP-1 targeted therapy, and evaluating therapeutic responses. - Source: PubMed
Publication date: 2025/12/01
Qiu FengshuangTang ShuangLiu XuweiLei JialiangBian LinjieZhang FengshengPan XiaoyuXu XiaopingHe SiminZhang JianpingLi JindianSong Shaoli - Glioblastoma multiforme (GBM) is an aggressive primary brain tumour associated with a poor prognosis despite standard-of-care treatment, including surgical resection, radiotherapy and temozolomide (TMZ) chemotherapy. Certepetide (also known as LSTA1, CEND-1) is an investigational tumour-penetrating peptide that facilitates the extravascular delivery and intratumoural penetration of co-administered immune/chemotherapeutics; however, it has not yet been evaluated in clinical trials for the treatment of intracranial malignancies. - Source: PubMed
Publication date: 2025/11/13
Truusalu Johannes PärtelOselin KerstiLass JanaBuck Kristen KSietsema WilliamSoeorg HiieToome KadriKaarna KatrinTeesalu TambetKõrgvee Lenne-Triin