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Disruption of DREAM and RB-E2F (zeige E2F1 ELISA Kits) complexes by oncoproteins from DNA tumor viruses leads to upregulation of cell cycle genes and impairs growth-inhibiting pathways, including the p53 (zeige TP53 ELISA Kits)-mediated downregulation of cell cycle genes. [review]
A relatively stable genome in retinoblastoma tumor cells is maintained by TRb1 (zeige TRIB1 ELISA Kits) and TRb2 (zeige TRIB2 ELISA Kits)-mediated PTTG1 (zeige PTTG1 ELISA Kits) inhibition, counteracting Rb-deficiency-related genomic instability.
APC/C and pRB interact with each other via the co-activator of APC/C, FZR1, providing an alternative pathway of regulation of G1 to S transition by pRB using a post-translational mechanism. Both pRB and FZR1 have complex roles and are implicated not only in regulation of cell proliferation but also in differentiation, quiescence, apoptosis, maintenance of chromosomal integrity and metabolism.
Analysis of the spectrum of RB1 variants observed in 60,706 exomes identifies 197 variants that have enough potential to disrupt splicing to warrant further consideration.
AR also indirectly increases the expression of DNA replication genes through stimulatory effects on other metabolic genes with subsequent CDK (zeige CDK4 ELISA Kits) activation and Rb hyperphosphorylation.
Results show that the functional state of protein Rb is inferred to be inactive due its phosphorylation status in the MYCN (zeige 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 (zeige 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 (zeige FAM126A ELISA Kits).
The data indicate that MAZ is essential to bypass MYB (zeige MYB ELISA Kits) promoter repression by RB family members and to induce MYB (zeige MYB ELISA Kits) expression.
RB inactivation enhances pro-inflammatory signaling through stimulation of the interleukin-6 (zeige IL6 ELISA Kits)/STAT3 (zeige STAT3 ELISA Kits) pathway, which directly promotes various malignant features of cancer cells. [review]
Findings indicate that inactivation of the Rb family proteins (Rb, p107 (zeige 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 (zeige SOCS3 ELISA Kits) protein (Socs3 (zeige SOCS3 ELISA Kits)) expression in triple knockout (TKO (zeige 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 (zeige E2F1 ELISA Kits) to recruit EZH2 (zeige EZH2 ELISA Kits) to diverse repeat sequences.
The N-Terminal phosphorylation of RB by p38 (zeige CRK ELISA Kits) bypasses its inactivation by cyclin (zeige PCNA ELISA Kits)-dependent kinases and prevents proliferation in cancer cells.
SUMO1 (zeige SUMO1 ELISA Kits) conjugation of RB and Lamin A/C (zeige LMNA ELISA Kits) is modulated by the SUMO protease SENP1 (zeige 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 (zeige CDK4 ELISA Kits) inhibitors releases Rb-mediated mTORC2 (zeige CRTC2 ELISA Kits) suppression. This, in turn, leads to elevated Akt (zeige AKT1 ELISA Kits) activation to confer resistance to chemotherapeutic drugs in Rb-proficient cells, which can be attenuated with Akt (zeige AKT1 ELISA Kits) inhibitors.
The data presented here support a hypothesis in which RB1 and TP53 (zeige TP53 ELISA Kits) loss in prostate cancer derepresses Ezh2 (zeige EZH2 ELISA Kits) and Sox2 (zeige SOX2 ELISA Kits) factors, creating a stem cell-like epigenetic environment permissive for lineage plasticity
systems-level control of cell cycle arrest by pRB (zeige PGR ELISA Kits)-E2F (zeige E2F1 ELISA Kits) and p27 (zeige CDKN1B ELISA Kits)-CDK (zeige CDK4 ELISA Kits) regulation, is reported.
RB is necessary for the recruitment of the BRG1 (zeige SMARCA4 ELISA Kits) ATPase (zeige 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 (zeige THOC2 ELISA Kits) ribonucleoprotein (zeige RBP31 ELISA Kits) complex.
Our results indicate that Rb-Raf-1 (zeige 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 (zeige USP37 ELISA Kits) regulates embryonic pituitary homeostasis by targeting rb1 and e2f4 (zeige 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