Rat AntiORC6 (origin recognition complex 6) Target Antigen ORC6 (origin recognition complex 6) Host Isotype Rat IgG2a Application ChIP; IP; WB;
- Known as:
- Rat AntiORC6 (origin recognition aggregate 6) Target Antigen ORC6 (origin recognition aggregate 6) Host Isotype Rat IgG2a Application ChIP; IP; Western Blot;
- Catalog number:
- IQ306
- Product Quantity:
- 50ul (1mg/ml)
- Category:
- -
- Supplier:
- Imunquest
- Gene target:
- Rat AntiORC6 (origin recognition complex 6) Target Antigen ORC6 Host Isotype IgG2a Application ChIP; ;
Ask about this productRelated genes to: Rat AntiORC6 (origin recognition complex 6) Target Antigen ORC6 (origin recognition complex 6) Host Isotype Rat IgG2a Application ChIP; IP; WB;
- Gene:
- ORC6 NIH gene
- Name:
- origin recognition complex subunit 6
- Previous symbol:
- ORC6L
- Synonyms:
- -
- Chromosome:
- 16q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-14
- Date modifiied:
- 2016-10-05
Related products to: Rat AntiORC6 (origin recognition complex 6) Target Antigen ORC6 (origin recognition complex 6) Host Isotype Rat IgG2a Application ChIP; IP; WB;
α - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(+)_Isopinocampheylborane tmeda complex(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Anti_Tg)Thyroglobulin Antigen Related articles to: Rat AntiORC6 (origin recognition complex 6) Target Antigen ORC6 (origin recognition complex 6) Host Isotype Rat IgG2a Application ChIP; IP; WB;
- Oral squamous cell carcinoma (OSCC) shows marked biological heterogeneity, but markers that connect malignant epithelial states with the tumor immune context remain limited. Origin recognition complex subunit 6 (ORC6) participates in DNA replication licensing, but its disease-specific role in OSCC is not well defined. - Source: PubMed
Publication date: 2026/07/21
Yan ShaofuTan WenqiZhang YanxinSi JinyanGuo JiehuaYang BoShi Jing - The human Origin Recognition Complex subunit 6 has recently garnered significant attention. The loss of human Orc6 doesn't impact MCM loading in vivo, while in vitro reconstitution experiments have demonstrated that MCM loading can occur without Orc6, though could be stimulated upon the addition of Orc6. We recently reported an unexpected role for hOrc6, in promoting S-phase progression post pre-RC assembly and DNA damage response (DDR). Using CUT&RUN to map the binding of Orc6 genome-wide, we find that Orc6 is present at replication origins and at sites of DNA damage during S-phase. Upon encountering oxidative damage in S-phase, Orc6 interacts with the chromatin remodelers, SMARCA1/SNF2L, also a component of the replication fork. Loss of Orc6 shows enhanced genome-wide association of SMARCA1 to Orc6-bound sites, concomitant with chromatin remodeling at these sites supporting the model that Orc6 is a negative regulator of SMARCA1 and constrains its localization. Upon DNA damage, enhanced association of Orc6 to SMARCA1 prevents chromatin remodeling activity to halt replication progression. We propose that during S-phase, Orc6 is a barrier factor, which limits the activity of chromatin remodelers. - Source: PubMed
Liu DazhenMishra MohitWang YouyangOishi HumayraMirza AneekMohajir Iman FatimahChetlangia NehaSonalkar JayLin Yo-ChuenPrasanth Kannanganattu VPrasanth Supriya G - Origin Recognition Complex Subunit 6 () is essential for DNA replication initiation. However, its dynamic expression patterns and potential biological functions during the progression of cervical lesions remain unclear. - Source: PubMed
Publication date: 2026/05/29
Chen RouyiHuang LuHuang YunChen FeihuZhong LijunOu FanyanYang YangWu Yinghui - Cervical cancer remains a major cause of cancer-related morbidity and mortality in women, particularly among patients diagnosed with locally advanced, recurrent, or metastatic disease. Here, we investigated the role of transcriptional repressor GATA-binding 1 (TRPS1) in cervical cancer progression and defined its downstream regulatory mechanism. Bioinformatics analysis revealed differential expression of TRPS1 between cervical cancer and normal cervical tissues. To further explore its functional role, TRPS1 was overexpressed in cervical cancer cell lines via lentiviral infection. In vitro and in vivo experiments confirmed that TRPS1 expression was downregulated in cervical cancer, and its overexpression inhibited cervical cancer cell proliferation, migration, invasion, and stemness, as well as tumor growth in xenograft models. Mechanistically, ORC6 was identified as a candidate downstream effector of TRPS1. TRPS1 bound to the ORC6 promoter and repressed ORC6 transcription, leading to reduced ORC6 expression. Functional rescue experiments showed that ORC6 restoration partially reversed TRPS1-mediated inhibition of cell-cycle progression, apoptosis resistance, stemness-marker expression, EMT-associated marker expression, and tumor growth. Notably, low TRPS1 expression and high ORC6 expression were associated with lymphovascular invasion and lymph node metastasis in cervical cancer patients. Together, these findings identify a TRPS1-ORC6 regulatory axis that restrains cervical cancer stemness and progression. - Source: PubMed
Publication date: 2026/05/30
He JuanYan RuyuDu YitongYang HuilingFeng YichenTian MinWu ZejunLi LeiXiang LanSun DuoxiangLi XianghuaZhou KechengZhuang Yali - With the application of precise clinical interventions in tumor treatment, it is of great value to explore novel biomarkers and their underlying molecular mechanisms. In this paper, we firstly explored the prognostic, immunological features, functions, and potential mechanisms of ORC6 in kidney renal clear cell carcinoma (KIRC) via single-cell and bulk RNA sequencing. Single-cell and bulk RNA sequencing data related to ORC6 data in KIRC were acquired from shared online databases. Spearman correlation analyses were carried out to investigate the relationships between ORC6 expression and interested targets, including tumor mutation burden (TMB), tumor microenvironment, and immunotherapy responses. Besides, the expression pattern of ORC6 and its role in KIRC were verified in vitro experiments. Also, the potential mechanisms and regulatory upstream of ORC6 in KIRC were explored. ORC6 was up-regulated in KIRC samples compared with normal tissues, validated by PCR analyses of KIRC tissues and cell lines (p < 0.05). Single-cell RNA sequencing analysis showed that ORC6 was mainly expressed in immune T cells. Survival and Cox regression analysis showed ORC6 had prognostic values in KIRC (p < 0.05). Correlation analysis revealed ORC6 was strongly correlated with immunity and immunotherapy sensitivity (p < 0.05). Further experiments in vitro indicated that ORC6 could regulate the cell proliferation/apoptosis of KIRC. Finally, a putative long non-coding RNA (LncRNA)/RNA binding protein (RBP)/ORC6 regulatory network was identified to explore ORC6-related potential upstream regulatory mechanisms in KIRC. In conclusion, ORC6 might play oncogenic roles in KIRC and regulate cell proliferation/apoptosis in KIRC. Furthermore, ORC6 showed significant associations with immunity and potential immunotherapy sensitivity. These findings provided a foundation for future studies evaluating the clinical significance of ORC6 in KIRC. - Source: PubMed
Yu YangZhai JingLiu ShiweiWang YiDing Guanxiong