Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Results show that ablation of the three members of the retinoblastoma family (RB1 (show RB1 Antibodies), p107 (show RBL1 Antibodies) 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.
Findings indicate that inactivation of the Rb family proteins (Rb, p107 (show RBL1 Antibodies), and p130) in hematopoietic stem cells (HSCs) progressively impairs their homeostasis, which is rescued upon repression of suppressor of cytokine signaling 3 (show SOCS3 Antibodies) protein (Socs3 (show SOCS3 Antibodies)) expression in triple knockout (TKO (show MRPS12 Antibodies)) HSCs.
Deletion of Rb or p130 leads to impaired repression of Sox2 (show SOX2 Antibodies), a defect amplified by inactivation of p53 (show TP53 Antibodies). Identify binding of pRb (show PGR Antibodies) and p130 to an enhancer with crucial regulatory activity on Sox2 (show SOX2 Antibodies) 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 Antibodies) family.
Following stress exposure, E2F4 (show E2F4 Antibodies)-p130 complexes are lost rapidly along with the presence of E2F4 (show E2F4 Antibodies) at E2F (show E2F1 Antibodies)-containing B-Myb (show MYBL2 Antibodies) promoter sites.
PRMT5 (show PRMT5 Antibodies) knockdown in non-Hodgkin lymphoma cell lines and primary lymphoma cells leads to RBL2 derepression and RB1 (show RB1 Antibodies) reactivation, which in turn inhibit PRC2 expression.
Rb, p107 (show RBL1 Antibodies) 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 Antibodies)) and BORIS (show CTCFL Antibodies) in T-antigen-positive but not in T-antigen-negative cells.
Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) and pRb (show PGR Antibodies) signal pathways interact with each other and form common p130/Gsk3beta/beta-catenin (show CTNNB1 Antibodies) complex during MSC (show MSC Antibodies) cycle progression.
UL97 phosphorylates and inactivates the retinoblastoma protein-related p107 (show RBL1 Antibodies) 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 Antibodies) induced RBL2 expression through down-regulating miR (show MLXIP Antibodies)-93 in renal cancer cells
the inactivation of RB1 (show RB1 Antibodies) 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 Antibodies)-106a and its family members were upregulated; findings suggest miR (show MLXIP Antibodies)-106a can repress expression of the retinoblastoma family member RBL2 and miR (show MLXIP Antibodies)-106a overexpression results in rapid tumor growth and poor differentiation
Low expression of RBL2 is associated with glioma.
Silencing of RB1 (show RB1 Antibodies) 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