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results showed that a) alterations of the p53 (Montrer TP53 Protéines) 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 (Montrer NFKB1 Protéines) p65 (Montrer GORASP1 Protéines)/miR17/RB pathway. As NF-kappaB (Montrer NFKB1 Protéines) p65 (Montrer GORASP1 Protéines) 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 (Montrer ODZ1 Protéines) stage.
According to immunohistochemistry and immunoblot analysis, the expression levels of cyclin D1 (Montrer CCND1 Protéines), cyclin E (Montrer CCNE1 Protéines), pRb, and Ki67 (Montrer MKI67 Protéines) 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 (Montrer TP53 Protéines) 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 (Montrer E2F1 Protéines) target genes as susceptible to the regulatory influence of H1.2 (Montrer HIST1H1C Protéines), where H1.2 (Montrer HIST1H1C Protéines) 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 (Montrer LIN37 Protéines) 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 (Montrer RBL1 Protéines) 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 (Montrer NFIB Protéines) overexpression interacts with Rb/p53 (Montrer TP53 Protéines) deletion to promote small cell lung cancer in a mouse model
studies demonstrate that pRb (Montrer PGR Protéines) loss in the Tie2 (Montrer TEK Protéines)-lineage that includes aortic valve interstitial cells is sufficient to cause age-dependent aortic valve dysfunction
Cytokeratin-19 (CK-19 (Montrer KRT19 Protéines))+ specific deletion of tumor suppressors p53 (Montrer TP53 Protéines) and Retinoblastoma (Rb) indicated that carcinomas at the injury site originates from cholangiocytes or liver progenitor cells.
Rb selectively inhibits innate IFN-beta (Montrer IFNB1 Protéines) production by enhancing deacetylation of Ifnb1 (Montrer IFNB1 Protéines) 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 (Montrer RBL1 Protéines), and p130) in hematopoietic stem cells (HSCs) progressively impairs their homeostasis, which is rescued upon repression of suppressor of cytokine signaling 3 (Montrer SOCS3 Protéines) protein (Socs3 (Montrer SOCS3 Protéines)) expression in triple knockout (TKO (Montrer MRPS12 Protéines)) HSCs.
Combined deletion of Vhl (Montrer VHL Protéines), Trp53 (Montrer TP53 Protéines) and Rb1 specifically in renal epithelial cells in mice caused clear cell renal cell carcinoma (Montrer MOK Protéines).
The evidence has been presented that the retinoblastoma protein utilizes a cell-cycle-independent interaction with E2F1 (Montrer E2F1 Protéines) to recruit EZH2 (Montrer EZH2 Protéines) to diverse repeat sequences.
data indicate that the Rb1-E2F1 (Montrer E2F1 Protéines)-caspase (Montrer CASP3 Protéines) axis is crucial for protecting immature T cells from apoptosis during early T lymphocyte maturation.
Our results indicate that Rb-Raf-1 (Montrer RAF1 Protéines) 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 (Montrer USP37 Protéines) regulates embryonic pituitary homeostasis by targeting rb1 and e2f4 (Montrer E2F4 Protéines) 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
, RNA-binding motif protein 45
, RNA-binding protein 45
, developmentally regulated RNA-binding protein 1
, developmentally-regulated RNA-binding protein 1
, putative RNA binding protein RB-1
, Retinoblastoma 1 (including osteosarcoma)
, retinoblastoma 1 (including osteosarcoma)
, retinoblastoma protein
, retinoblastoma, susceptibility
, Retinoblastoma-associated protein
, retinoblastoma 1
, retinoblastoma-associated protein-like