MCM4 antibody - middle region (ARP36649_T100)
- Known as:
- MCM4 (anti-) - middle region (ARP36649_T100)
- Catalog number:
- arp36649_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MCM4 antibody - middle region (ARP36649_T100)
Related genes to: MCM4 antibody - middle region (ARP36649_T100)
- Gene:
- MCM4 NIH gene
- Name:
- minichromosome maintenance complex component 4
- Previous symbol:
- CDC21
- Synonyms:
- CDC54, hCdc21, P1-Cdc21, MGC33310
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
Related products to: MCM4 antibody - middle region (ARP36649_T100)
Related articles to: MCM4 antibody - middle region (ARP36649_T100)
- Potato spindle tuber viroid (PSTVd) infection can induce tuber cracking and knob-like protuberances at tuber eyes, but the molecular differences between these two localized symptoms remain unclear. In this study, smooth surface regions and normal eye tissues were collected from mock-inoculated tubers of the potato cultivar 'Kexin 18', whereas crack regions and regions of knob-like protuberances at tuber eyes were collected from PSTVd-infected tubers. RNA sequencing and targeted phytohormone quantification were combined with weighted gene co-expression network analysis, infection × region interaction analysis, and gene-hormone association analysis. PSTVd infection markedly inhibited plant growth and tuber development, and 2972 genes with significant infection × region interaction effects were identified. Crack regions were characterized primarily by enhanced defense and oxidative stress related transcriptional responses, remodeling of cell wall and surface barrier related processes, and accumulation of several cytokinin (CK) metabolites, salicylic acid/salicylic acid glucoside (SA/SAG), and 12-oxo-phytodienoic acid (OPDA); , , and were among the representative candidate genes. Regions of knob-like protuberances at tuber eyes showed pronounced reprogramming of processes related to DNA replication, the cell cycle, chromosome maintenance, and chromatin organization, together with decreases in several CK metabolites, a downward trend in jasmonate-related oxylipins, and an increase in indole-3-butyric acid; , , , and were identified as candidate genes. Gene-hormone association analysis further revealed distinct molecular association patterns in the two regions. Collectively, the two symptomatic regions exhibited distinct region-dependent transcriptomic and phytohormone metabolic states after symptom development. - Source: PubMed
Publication date: 2026/09/17
Li GuangyanHussain WajahatPan TingChen YingyanLi JiaqiZeng YunxiaZhou YonghongLv Dianqiu - Regulated helicase activation by DDK kinase is central for genome stability. However, how DDK phosphorylation primes the MCM2-7 double hexamer (DH) for Sld3-Sld7 binding and Cdc45 loading remained unclear. We define this mechanism through cryo-EM structures of MCM2-7 DH-Sld3-Sld7 (MS) and MCM2-7 DH-Sld3-Sld7-Cdc45 (MSC). We reveal that the autoinhibitory Mcm4 tail engages not only Mcm4 but also Mcm6. Upon DDK-dependent phosphorylation, both of these sites become accessible. In the context of the MS structure, we identify that two short Sld3 motifs that contact Mcm4 and Mcm6 read out the DH phosphorylation state, while the Sld3 Treslin domain (STD) binds to Mcm2. In the MSC structure, Cdc45 dislodges the Sld3 STD from Mcm2, allowing Sld3 to position Cdc45 at the Mcm2/Mcm5 interface. Mutagenesis of the Sld3 STD-Cdc45 interface disrupts Cdc45 loading, validating this interaction. Together, our data reveal a phosphorylation-encoded mechanism coupling DDK-activated Mcm4/Mcm6 surfaces to distal Cdc45 placement, explaining how firing factors choreograph the DH-to-CMG transition. - Source: PubMed
Publication date: 2026/08/14
Noguchi YasunoriSaleh AlmutasemSchneider SarahIvanova Marina EChen Zhuo AngelRanjha LepakshiAramayo RicardoTognetti SilviaFaull Sarah VRappsilber JuriSpeck Christian - EIF1, an RNA-binding protein implicated in multiple diseases, remains poorly characterized in diabetic retinopathy (DR). This study therefore investigated EIF1 expression and function in an in vitro model of DR pathogenesis. - Source: PubMed
Publication date: 2026/09/03
Li NaMa QianFan XinLiu QiLiu LiZhang ShengfuMa YalingXu HongxiaLi Xinyi - Hereditary adrenocortical unresponsiveness to adrenocorticotropin (HAUA) is a rare congenital disorder characterized by isolated glucocorticoid deficiency with preserved mineralocorticoid production. HAUA encompasses familial glucocorticoid deficiency (FGD) and triple A syndrome (AAAS) and is caused by autosomal recessive defects in ACTH-signaling-related genes, including MC2R, MRAP, AAAS, NNT, TXNRD2, and MCM4. To clarify the current clinical characteristics of HAUA (including FGD and AAAS) in Japan, we conducted a nationwide questionnaire-based survey. The primary survey identified the number of affected patients, and the secondary survey collected detailed clinical information. Fifteen patients were identified from 12 institutions. Detailed clinical data were obtained from nine patients (mean age, 40.6 years). Most patients developed symptoms during childhood [3.75 (0-8) years]. Seven presented with chronic adrenal insufficiency, and two experienced life-threatening events, hypoglycemia or encephalopathy. Genetic confirmation was obtained in four cases. All patients received glucocorticoid replacement therapy (mean hydrocortisone-equivalent dose, 13.0 mg/m/day). Notably, 50% of adult patients were obese (BMI ≥25 kg/m), although no clear association between glucocorticoid dose and BMI was observed. Despite the limited cohort size, this study provides detailed clinical information on HAUA (including FGD and AAAS) in Japan and suggests a potential risk of obesity in long-term management. - Source: PubMed
Publication date: 2026/08/11
Tanimoto EriKashimada KenichiMatsuura BunzoYamaguchi HidekiKurajoh MasafumiSegawa ToshieOhba KenjiAbe YukiWada YasunoriKanno JunkoOda YoichiroTajima ToshihiroShibata HirotakaHasegawa Tomonobu - Familial glucocorticoid deficiency (FGD) is a rare autosomal recessive disorder characterized by isolated cortisol deficiency and elevated adrenocorticotropic hormone (ACTH) levels. Variants in , which encodes mitochondrial thioredoxin reductase 2, have recently been implicated in FGD; however, the phenotypic and mutational spectrum remain extremely limited. - Source: PubMed
Publication date: 2026/05/28
Al Alwan IbrahimAlhamoudi Kheloud MAlzaben Abdullah IbrahimAlmulhem BeshaierQawasmi NawalAlswailem MeshaelAlotaibi SaraAlsaihati BurairJabaan AmjadMahzari MoeberFlück Christa EAlzahrani Ali S