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Concurrent mutations, in genes such as CDKN2B or RB1, were associated with worse clinical outcome in lung adenocarcinoma patients with EGFR active mutations.
Mutational screening of germline RB1 gene in Vietnamese patients with retinoblastoma reveals three novel mutations.
Analyses with phospho-defective and phospho-mimetic mutants of FoxM1b identified a critical role of the Plk1 phosphorylation sites in regulating the binding of FoxM1b to Rb and DNMT3b.
The accumulation of sequence variations in RB1 gene might influence Greek patients' susceptibility towards the progression of cervical neoplasia.
vitiligo lesions exhibited dysregulated SUMOylation and deSUMOylation in keratinocytes, dysregulation of the cell cycle progression was observed in SUMO1 knockdown HaCaT cells and the deSUMOylation of Rb in keratinocytes may serve an important role in the development of vitiligo.
The Rb1 tumor suppressor gene modifies telomeric chromatin architecture by regulating TERRA expression.
These findings demonstrate that developmental stage-specific as well as species- and cell type-specific features sensitize to RB1 inactivation and reveal the human cone precursors' capacity to model retinoblastoma initiation, proliferation, premalignant arrest, and tumor growth.
Low pRB expression is associated with mouth Cancer.
Control of the Restriction Point by Rb and p21.
PPM1B plays a negative role in the activation of the p38-RB1-E2F1 pathway and that targeting PPM1B could be useful in certain types of cancer by stimulating chemotherapy-induced cell death.
results showed that a) alterations of the p53 and Rb pathways are associated with high proliferation of tumor cells in BUC and b) high expression of cell-cycle proteins is associated with adverse histopathological parameters of these tumors
he present result indicated that vascular smooth proliferation is regulated by activation of the NF-kappaB p65/miR17/RB pathway. As NF-kappaB p65 signalling is activated in and is a master regulator of the inflammatory response, the present findings may provide a mechanism for the excessive proliferation of VSMCs under inflammation during vascular disorders and may identify novel targets for the treatment of vascular d...
Reduced RB expression in medullary thyroid cancer is associated with decreased patient survival in univariate and multivariable analyses, independent from patient age at surgery or advanced TNM stage.
According to immunohistochemistry and immunoblot analysis, the expression levels of cyclin D1, cyclin E, pRb, and Ki67 in psoriasis lesions decreased after treatment and were similar with those in the normal group
Data indicate that nuclear envelope rupture in cancer cells is likely due to loss of either the Rb or the p53 pathway.
Altered pRb is frequently expressed in gastric carcinoma, inversely correlates with tumor invasion and tumor stage suggesting an early event in gastric carcinogenesis.
results define a network of E2F target genes as susceptible to the regulatory influence of H1.2, where H1.2 augments global association of pRb with chromatin, enhances transcriptional repression by pRb, and facilitates pRb-dependent cell-cycle arrest
The increased expression of miR-503-5p significantly reduced the expressions of E2F transcription factor 3 (E2F3) mRNA and retinoblastoma protein (Rb)/E2F signaling pathway mRNA in bladder cancer cells.
Loss of Rb immunolabeling and KRAS mutation are promising molecular markers of the therapeutic response to platinum-based chemotherapy for pancreatic neuroendocrine neoplasm grade-3 (PanNEN-G3), and Rb for neuroendocrine tumor with G3 (NET-G3).
We recommend intensive ocular screening for patients with germline RB1 mutations for retinoblastoma as well as neuroimaging for pineoblastoma surveillance. There is an approximately 20% risk of developing second primary cancers among individuals with hereditary RB, higher among those who received radiotherapy for their primary RB tumors
Thus, Lin37 is an essential component of DREAM complex that cooperates with Rb to induce quiescence.
Results show that ablation of the three members of the retinoblastoma family (RB1, p107 and p130) which targets a variety of adult lung epithelial cells, leads to spontaneous velopment of tumorlets, benign precancerous neuroendocrine (NE) lesions that do not progress to malignant tumors. Data imply the requirement of other oncogenic signaling pathways for full transformation in NE lung lesions mutant for the Rb family.
NFIB overexpression interacts with Rb/p53 deletion to promote small cell lung cancer in a mouse model
studies demonstrate that pRb loss in the Tie2-lineage that includes aortic valve interstitial cells is sufficient to cause age-dependent aortic valve dysfunction
Cytokeratin-19 (CK-19)+ specific deletion of tumor suppressors p53 and Retinoblastoma (Rb) indicated that carcinomas at the injury site originates from cholangiocytes or liver progenitor cells.
These results demonstrate a crucial role for RB in the generation and the survival of DGCs in the embryonic and the adult brain.
Rb selectively inhibits innate IFN-beta production by enhancing deacetylation of Ifnb1 promoter, exhibiting a previous unknown non-classical role in innate immunity, which also suggests a role of Rb in the regulation of type I IFN production in inflammatory or autoimmune diseases.
Epithelial IGF1R is dispensable for IGF2-mediated enhanced intestinal adaptation after small bowel resection in retinoblastoma-deficient mice.
Findings indicate that inactivation of the Rb family proteins (Rb, p107, and p130) in hematopoietic stem cells (HSCs) progressively impairs their homeostasis, which is rescued upon repression of suppressor of cytokine signaling 3 protein (Socs3) expression in triple knockout (TKO) HSCs.
Combined deletion of Vhl, Trp53 and Rb1 specifically in renal epithelial cells in mice caused clear cell renal cell carcinoma.
The evidence has been presented that the retinoblastoma protein utilizes a cell-cycle-independent interaction with E2F1 to recruit EZH2 to diverse repeat sequences.
The N-Terminal phosphorylation of RB by p38 bypasses its inactivation by cyclin-dependent kinases and prevents proliferation in cancer cells.
SUMO1 conjugation of RB and Lamin A/C is modulated by the SUMO protease SENP1 and that sumoylation of both proteins is required for their interaction.
Inhibition of Rb phosphorylation by depleting cyclin D or using CDK4/6 inhibitors releases Rb-mediated mTORC2 suppression. This, in turn, leads to elevated Akt activation to confer resistance to chemotherapeutic drugs in Rb-proficient cells, which can be attenuated with Akt inhibitors.
The data presented here support a hypothesis in which RB1 and TP53 loss in prostate cancer derepresses Ezh2 and Sox2 factors, creating a stem cell-like epigenetic environment permissive for lineage plasticity
Findings reveal that Rb deficiency accelerated urinary bladder cancer progression, exposing an important role of Rb in suppressing urinary bladder cancer for treatment in the future.
systems-level control of cell cycle arrest by pRB-E2F and p27-CDK regulation, is reported.
RB is necessary for the recruitment of the BRG1 ATPase to DNA double-strand breaks, which stimulates DNA end resection and homologous recombination
data indicate that the Rb1-E2F1-caspase axis is crucial for protecting immature T cells from apoptosis during early T lymphocyte maturation.
Our results indicate that Rb-Raf-1 interaction plays an important role in spontaneous hair cell regeneration in zebrafish
our analysis of zebrafish rb1 mutants reveals a previously unknown yet critical role for rb1 during retinotectal tract development and visual function.
Zebrafish usp39 regulates embryonic pituitary homeostasis by targeting rb1 and e2f4 expression, respectively, contributing to increased adenohypophyseal sensitivity to these altered cell cycle regulators
The protein encoded by this gene is a negative regulator of the cell cycle and was the first tumor suppressor gene found. The encoded protein also stabilizes constitutive heterochromatin to maintain the overall chromatin structure. The active, hypophosphorylated form of the protein binds transcription factor E2F1. Defects in this gene are a cause of childhood cancer retinoblastoma (RB), bladder cancer, and osteogenic sarcoma.
retinoblastoma suspectibility protein
, retinoblastoma-associated protein
, retinoblastoma-like protein 1
, Retinoblastoma 1 (including osteosarcoma)
, retinoblastoma 1 (including osteosarcoma)
, retinoblastoma protein
, retinoblastoma, susceptibility
, Retinoblastoma-associated protein
, retinoblastoma 1
, retinoblastoma-associated protein-like