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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.
Deletion of Rb or p130 leads to impaired repression of Sox2 (show SOX2 ELISA Kits), a defect amplified by inactivation of p53 (show TP53 ELISA Kits). Identify binding of pRb (show PGR ELISA Kits) and p130 to an enhancer with crucial regulatory activity on Sox2 (show SOX2 ELISA Kits) 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 ELISA Kits) family.
Following stress exposure, E2F4 (show E2F4 ELISA Kits)-p130 complexes are lost rapidly along with the presence of E2F4 (show E2F4 ELISA Kits) at E2F (show E2F1 ELISA Kits)-containing B-Myb (show MYBL2 ELISA Kits) promoter sites.
PRMT5 (show PRMT5 ELISA Kits) knockdown in non-Hodgkin lymphoma cell lines and primary lymphoma cells leads to RBL2 derepression and RB1 (show RB1 ELISA Kits) reactivation, which in turn inhibit PRC2 expression.
Rb, p107 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 ELISA Kits)) and BORIS (show CTCFL ELISA Kits) in T-antigen-positive but not in T-antigen-negative cells.
Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) and pRb (show PGR ELISA Kits) signal pathways interact with each other and form common p130/Gsk3beta (show GSK3b ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) complex during MSC (show MSC ELISA Kits) cycle progression.
Mutation of p107 or p130 reduces survival of Rb-deficient myoblasts during differentiation.
UL97 phosphorylates and inactivates the retinoblastoma protein-related p107 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 ELISA Kits) induced RBL2 expression through down-regulating miR (show MLXIP ELISA Kits)-93 in renal cancer cells
the inactivation of RB1 (show RB1 ELISA Kits) 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 ELISA Kits)-106a and its family members were upregulated; findings suggest miR (show MLXIP ELISA Kits)-106a can repress expression of the retinoblastoma family member RBL2 and miR (show MLXIP ELISA Kits)-106a overexpression results in rapid tumor growth and poor differentiation
Low expression of RBL2 is associated with glioma.
Silencing of RB1 (show RB1 ELISA Kits) 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