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Concurrent HR deficiency and RB1 loss were associated with favorable outcomes, suggesting that co-occurrence of specific mutations might mediate durable responses in such patients
miR-199a-3p is down-regulated in rheumatoid arthritis (RA)-Fibroblast-like synoviocytes (FLSs)(RA-FLS) and miR-199a-3p inhibits proliferation and induces apoptosis in , partially via targetting RB1. The miR-199a-3p/RB1 pathway may represent a new therapeutic target for RA.
this study shows that pRb loss emerged as the most significant poor prognostic indicator in conjunctival squamous cell carcinoma
RB activation signals are integrated in a phosphorylation code that determines the diversity of RB activity.
RASSF6 increases unphosphorylated pRb and augments the interaction between pRb and E2F1. Moreover, RASSF6 induces TP73 target genes via pRb and E2F1 in a p53-negative background.
BMP-2 is a driving factor for promoting epithelial mesenchymal transition and breast cancer stemness via Rb and CD44 signaling pathways
The authors report that a subset of cell cycle-related genes including retinoblastoma 1 is the target of Rbfox2 in cytoplasmic stress granules, and Rbfox2 regulates the retinoblastoma 1 mRNA and protein expression levels during and following stress exposure.
Spectrum of germline RB1 mutations and clinical manifestations in retinoblastoma patients from Thailand have been reported.
these findings not only identify tumor-suppressive functions of RB that are distinct from cell cycle control, but also demonstrate that the molecular consequence of RB loss is distinct from RB inactivation.
The two most common deletions were tumor-suppressor genes RB1 and ERBB4 in chromophobe renal cell carcinoma but not renal oncocytoma.
a biomarker consisting of the phosphorylation of the retinoblastoma protein (Rb) on serine 249 combined with elevated p39 expression. This biomarker correlates with epithelial-to-mesenchymal transition traits in non-small cell lung carcinoma (NSCLC) cells.
E3 ubiquitin ligase RNF123 targets LMNB1, Rb protein and LAP2alpha for proteasomal degradation.
Mutation in RB1 gene is not associated with age at diagnosis for unilateral retinoblastoma.
the effects of combination treatment of phosphatase activation with TKIs on cell number and activation of the signal transducer and activator of transcription 3 (STAT3) resistance pathway were determined. The combination of Rb phosphatase activation with TKIs resulted in a greater reduction in cell number compared with either treatment alone, without STAT3 pathway activation.
Promoter hypermethylation was detected in 11.4% of the retinoblastoma tumors and should be tested for in routine RB1 screening programmes.
In conclusion, a novel low penetrance deep intronic variant within RB1 intron 18 was discovered (c.1814 + 1307C>G). Confirmation of the RB1 pathogenic variant and the low penetrance status assisted in surveillance scheduling and pregnancy management for this family.
No correlation was found between RB1germline mutations and second primary malignancies in hereditary retinoblastoma. EBRT treated patients with a low penetrance RB1 mutation remain at risk of second primary malignancies.
Previous evidences of a ~3-fold excess of RB1 maternal canonical transcript led us to hypothesize that this differential allelic expression could influence phenotypic outcome in families at risk for Retinoblastoma onset
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.
SUV39H1/DNMT3A-dependent methylation of the RB1 promoter stimulates PIN1 expression and melanoma development.
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.
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.
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