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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.
Deletion of Rb or p130 leads to impaired repression of Sox2 (show SOX2 Proteins), a defect amplified by inactivation of p53 (show TP53 Proteins). Identify binding of pRb (show PGR Proteins) and p130 to an enhancer with crucial regulatory activity on Sox2 (show SOX2 Proteins) expression.
In skeletal dysplasias cell cycle progression is compromised in the G1 phase due to reduced phosphorylation of the pocket protein p130 leading to inhibition of transcription factors of the E2F (show E2F1 Proteins) family.
Following stress exposure, E2F4 (show E2F4 Proteins)-p130 complexes are lost rapidly along with the presence of E2F4 (show E2F4 Proteins) at E2F (show E2F1 Proteins)-containing B-Myb (show MYBL2 Proteins) promoter sites.
PRMT5 (show PRMT5 Proteins) knockdown in non-Hodgkin lymphoma cell lines and primary lymphoma cells leads to RBL2 derepression and RB1 (show RB1 Proteins) reactivation, which in turn inhibit PRC2 expression.
Rb, p107 (show RBL1 Proteins) and p130 epigenetically protect newly born cortical neurons from DNA damage and cell division
The balance between phosphorylation and acetylation of Rb2/p130 is essential for its biological function in cell cycle control.
Rb2 coimmunolocalizes with the chromatin insulator CCCTC-binding factor (CTCF (show CTCF Proteins)) and BORIS (show CTCFL Proteins) in T-antigen-positive but not in T-antigen-negative cells.
Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) and pRb (show PGR Proteins) signal pathways interact with each other and form common p130/Gsk3beta/beta-catenin (show CTNNB1 Proteins) complex during MSC (show MSC Proteins) cycle progression.
Mutation of p107 (show RBL1 Proteins) or p130 reduces survival of Rb-deficient myoblasts during differentiation.
UL97 phosphorylates and inactivates the retinoblastoma protein-related p107 (show RBL1 Proteins) and p130 proteins
Hepatitis C virus core protein modulates pRb2/p130 expression in human hepatocellular carcinoma cell lines through promoter methylation
Statistical analysis revealed that Rbl2/p130 expression negatively correlates to its promoter methylation (r = -0.412) in tumor tissues.
TGF-beta (show TGFB1 Proteins) induced RBL2 expression through down-regulating miR (show MLXIP Proteins)-93 in renal cancer cells
the inactivation of RB1 (show RB1 Proteins) or RB2/P130 in uncommitted bone marrow stromal cells facilitates the first steps of adipogenesis.
expression profiling of miRNAs in high-grade serous ovarian carcinoma indicated miR (show MLXIP Proteins)-106a and its family members were upregulated; findings suggest miR (show MLXIP Proteins)-106a can repress expression of the retinoblastoma family member RBL2 and miR (show MLXIP Proteins)-106a overexpression results in rapid tumor growth and poor differentiation
Low expression of RBL2 is associated with glioma.
Silencing of RB1 (show RB1 Proteins) but not RB2/P130 decreases proliferative activity and impairs the differentiation potential of human mesenchymal stem cells.
Our hypothesis not only enrich the knowledge of the regulation of ALT, but also indicate that p130 may serve as a potential suppressor of ALT, and gene therapy of p130 may be used in cervical cancers.
Key regulator of entry into cell division. Directly involved in heterochromatin formation by maintaining overall chromatin structure and, in particular, that of constitutive heterochromatin by stabilizing histone methylation. Recruits and targets histone methyltransferases SUV420H1 and SUV420H2, leading to epigenetic transcriptional repression. Controls histone H4 'Lys-20' trimethylation. Probably acts as a transcription repressor by recruiting chromatin-modifying enzymes to promoters. Potent inhibitor of E2F-mediated trans-activation, associates preferentially with E2F5. Binds to cyclins A and E. Binds to and may be involved in the transforming capacity of the adenovirus E1A protein. May act as a tumor suppressor.
retinoblastoma-like 2 (p130)
, retinoblastoma-like protein 2
, retinoblastoma-like protein 2-like
, Retinoblastoma-related protein 2
, retinoblastoma-related protein 2a
, 130 kDa retinoblastoma-associated protein
, retinoblastoma-related protein 2
, PPAR-alpha-interacting complex protein 128