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Results show that the functional state of protein Rb is inferred to be inactive due its phosphorylation status in the MYCN (show MYCN ELISA Kits)-amplified retinoblastoma without coding sequence mutations. This makes inactivation of RB1 by gene mutation or by protein phosphorylation, a necessary condition for initiating retinoblastoma tumorigenesis, independent of MYCN (show MYCN ELISA Kits) amplification.
Loss of RB1 is associated with papillomavirus involvement in Barrett's dysplasia and esophageal adenocarcinoma.
The epigenetic interaction between Linc00441 and bidirectional transcripted neighbor RB1 may be a de novo theory cutting-point for the inactivation of RB1 in HCC (show FAM126A ELISA Kits).
The data indicate that MAZ is essential to bypass MYB (show MYB ELISA Kits) promoter repression by RB family members and to induce MYB (show MYB ELISA Kits) expression.
RB inactivation enhances pro-inflammatory signaling through stimulation of the interleukin-6 (show IL6 ELISA Kits)/STAT3 (show STAT3 ELISA Kits) pathway, which directly promotes various malignant features of cancer cells. [review]
RB1 deficiency promotes cancer cell proliferation in part by enhancing mitochondrial function and identify tigecycline as a clinically approved drug for RB1-deficient triple negative breast cancer.
this paper shows that patients with estrogen receptor (show ESR1 ELISA Kits) positive breast cancer expressing high Rb loss-of-function have significantly worse recurrence free survival compared to those with low Rb loss-of-function
Combinatorial PX-866 and Raloxifene Decrease Rb Phosphorylation, Cyclin E2 (show CCNE2 ELISA Kits) Transcription, and Proliferation of MCF-7 Breast Cancer Cells
TYROBP (show TYROBP ELISA Kits) influences a batch of genes that are related to Alzheimer's disease; ZNF329 and RB1 significantly regulate those 'mesenchymal' gene expression signature genes for brain tumors. By merely leveraging gene expression data, Context Based Dependency Network (CBDN) can efficiently infer the existence of gene-gene interactions as well as their regulatory directions.
Specific E2Fs also have prognostic value in breast cancer, independent of clinical parameters. We discuss here recent advances in understanding of the RB-E2F (show E2F1 ELISA Kits) pathway in breast cancer. We also discuss the application of genome-wide genetic screening efforts to gain insight into synthetic lethal interactions of CDK4/6 (show CDK4 ELISA Kits) inhibitors in breast cancer for the development of more effective combination therapies.
Findings indicate that inactivation of the Rb family proteins (Rb, p107 (show RBL1 ELISA Kits), and p130) in hematopoietic stem cells (HSCs) progressively impairs their homeostasis, which is rescued upon repression of suppressor of cytokine signaling 3 (show SOCS3 ELISA Kits) protein (Socs3 (show SOCS3 ELISA Kits)) expression in triple knockout (TKO (show MRPS12 ELISA Kits)) 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 (show E2F1 ELISA Kits) to recruit EZH2 (show EZH2 ELISA Kits) to diverse repeat sequences.
The N-Terminal phosphorylation of RB by p38 (show CRK ELISA Kits) bypasses its inactivation by cyclin (show PCNA ELISA Kits)-dependent kinases and prevents proliferation in cancer cells.
SUMO1 (show SUMO1 ELISA Kits) conjugation of RB and Lamin A/C (show LMNA ELISA Kits) is modulated by the SUMO protease SENP1 (show SENP1 ELISA Kits) and that sumoylation of both proteins is required for their interaction.
Inhibition of Rb phosphorylation by depleting cyclin D or using CDK4/6 (show CDK4 ELISA Kits) inhibitors releases Rb-mediated mTORC2 (show CRTC2 ELISA Kits) suppression. This, in turn, leads to elevated Akt (show AKT1 ELISA Kits) activation to confer resistance to chemotherapeutic drugs in Rb-proficient cells, which can be attenuated with Akt (show AKT1 ELISA Kits) inhibitors.
The data presented here support a hypothesis in which RB1 and TP53 (show TP53 ELISA Kits) loss in prostate cancer derepresses Ezh2 (show EZH2 ELISA Kits) and Sox2 (show SOX2 ELISA Kits) factors, creating a stem cell-like epigenetic environment permissive for lineage plasticity
systems-level control of cell cycle arrest by pRB (show PGR ELISA Kits)-E2F (show E2F1 ELISA Kits) and p27 (show CDKN1B ELISA Kits)-CDK (show CDK4 ELISA Kits) regulation, is reported.
RB is necessary for the recruitment of the BRG1 (show SMARCA4 ELISA Kits) ATPase (show DNAH8 ELISA Kits) to DNA double-strand breaks, which stimulates DNA end resection and homologous recombination
Findings implicate Rb1 in the regulation of the THO (show THOC2 ELISA Kits) ribonucleoprotein (show RBP31 ELISA Kits) complex.
Our results indicate that Rb-Raf-1 (show RAF1 ELISA Kits) 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 (show USP37 ELISA Kits) regulates embryonic pituitary homeostasis by targeting rb1 and e2f4 (show E2F4 ELISA Kits) 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