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Results show that RB1 expression is regulated by cdc37 (show CDC37 Proteins) which facilitates its phosphorylation through increasing CDK4 (show CDK4 Proteins) stability.
SOX2 (show SOX2 Proteins) overexpression and the loss of Rb1 protein expression might have a pivotal role in the divergent differentiation of pluripotent embryonic-like epithelial cells and the development of esophageal small-cell carcinoma.
several RB1 alterations associated to retinoblastoma in the human were present in several non-human primates without an apparent pathological effect.
Results suggest that RB1 is the dominant tumor suppressor PP in MCC (show MCC Proteins), and that inactivation of RB1 by MCPyV-LT is largely sufficient for its growth supporting function in established MCPyV-positive MCC (show MCC Proteins) cells.
the frequency and association of polymorphisms in the TP53 (show TP53 Proteins) and RB1 genes with clinical characteristics in a group of children with retinoblastoma (RB) in northern Mexico, was examined.
Results suggest that RBM45 (show RBM45 Proteins) serves as a negative regulator to prevent FUS (show FUS Proteins)-mediated excessive recruitment of HDAC1 (show HDAC1 Proteins) to the sites of DNA damage.
Authors show that MYC (show MYC Proteins) inhibition by Omomyc, a dominant-negative MYC (show MYC Proteins), suppresses the growth of SCLC cells with TP53 (show TP53 Proteins) and RB1 inactivation carrying MYC (show MYC Proteins), MYCL, or MYCN (show MYCN Proteins) amplification.
Data suggest that the platelet derived growth factor receptor alpha (show PDGFRA Proteins) (PDGFRalpha)/Stat3 (show STAT3 Proteins) transcription factor/Rb1 protein regulatory axis might represent a potential therapeutic target for glioblastoma (GBM) treatment.
miR (show MLXIP Proteins)-590 inhibits RB1 and promotes proliferation and invasion of T-cell acute lymphoblastic leukaemia cells
causative RB1 mutations in most bilateral retinoblastoma (RB) patients and in some unilateral RB patients, including five novel mutations, were identified.
Results show that ablation of the three members of the retinoblastoma family (RB1, p107 (show RBL1 Proteins) 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 (show NFIB Proteins) overexpression interacts with Rb/p53 (show TP53 Proteins) deletion to promote small cell lung cancer in a mouse model
studies demonstrate that pRb (show PGR Proteins) loss in the Tie2 (show TEK Proteins)-lineage that includes aortic valve interstitial cells is sufficient to cause age-dependent aortic valve dysfunction
Cytokeratin-19 (CK-19 (show KRT19 Proteins))+ specific deletion of tumor suppressors p53 (show TP53 Proteins) and Retinoblastoma (Rb) indicated that carcinomas at the injury site originates from cholangiocytes or liver progenitor cells.
Rb selectively inhibits innate IFN-beta (show IFNB1 Proteins) production by enhancing deacetylation of Ifnb1 (show IFNB1 Proteins) 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 (show RBL1 Proteins), and p130) in hematopoietic stem cells (HSCs) progressively impairs their homeostasis, which is rescued upon repression of suppressor of cytokine signaling 3 (show SOCS3 Proteins) protein (Socs3 (show SOCS3 Proteins)) expression in triple knockout (TKO (show MRPS12 Proteins)) HSCs.
Combined deletion of Vhl (show VHL Proteins), Trp53 (show TP53 Proteins) and Rb1 specifically in renal epithelial cells in mice caused clear cell renal cell carcinoma (show MOK Proteins).
The evidence has been presented that the retinoblastoma protein utilizes a cell-cycle-independent interaction with E2F1 (show E2F1 Proteins) to recruit EZH2 (show EZH2 Proteins) to diverse repeat sequences.
The N-Terminal phosphorylation of RB by p38 (show CRK Proteins) bypasses its inactivation by cyclin (show PCNA Proteins)-dependent kinases and prevents proliferation in cancer cells.
Our results indicate that Rb-Raf-1 (show RAF1 Proteins) 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 Proteins) regulates embryonic pituitary homeostasis by targeting rb1 and e2f4 (show E2F4 Proteins) 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-like protein 1
, Retinoblastoma 1 (including osteosarcoma)
, retinoblastoma 1 (including osteosarcoma)
, retinoblastoma protein
, retinoblastoma, susceptibility
, Retinoblastoma-associated protein
, retinoblastoma 1
, retinoblastoma-associated protein-like