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Study found that the methylation of global DNA decreased gradually after irradiation, and the methylation of the promoter of RBL1 gene may play an important role in the induction of radioresistance for three dimensional cultured carcinoma cells.
These findings in human skeletal muscle suggest that attenuated transcriptional repression through p107 may be a novel mechanism by which exercise stimulates mitochondrial biogenesis following exercise.
The authors found that phosphorylation of residues S650 and S975 in p107 weakens the E2F4 (show E2F4 Proteins) transactivation domain binding.
UL97 phosphorylates and inactivates the retinoblastoma protein-related p107 and p130 (show RBL2 Proteins) proteins
Sequence analysis of the RB1 (show RB1 Proteins) gene detected a novel mutation in bilateral retinoblastoma.
MAGE (show MAGEB10 Proteins)-A11 is a proto-oncogene (show RAB1A Proteins) whose increased expression in prostate cancer reverses retinoblastoma-related protein p107 from a transcriptional repressor to a transcriptional activator of the androgen receptor (show AR Proteins) and E2F1 (show E2F1 Proteins).
Single nucleotide polymorphism in the ultraconserved elements of RBL1 gene is associated with recurrence in colorectal adenocarcinoma.
Concomitant germline large cytogenetic 13q deletion and somatic mutations in the RB1 (show RB1 Proteins) gene in unilateral retinoblastoma.
identification of a PP2A (show PPP2R4 Proteins) trimeric holoenzyme containing B55alpha (show PPP2R2A Proteins), which plays a major role in restricting the phosphorylation state of p107 and inducing its activation in human cells.
regulation of expression of p130 (show RBL2 Proteins), p107 and E2F-4 (show E2F4 Proteins) in human cells
Results show that ablation of the three members of the retinoblastoma family (RB1 (show RB1 Proteins), 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.
the transcriptional corepressor p107 orchestrates a metabolic checkpoint that determines adipocyte lineage fates for non-committed progenitors.
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 (show SOCS3 Proteins) protein (Socs3 (show SOCS3 Proteins)) expression in triple knockout (TKO (show MRPS12 Proteins)) HSCs.
p107 is required for the efficient recruitment of an activating SWI (show SMARCA1 Proteins)/SNF (show SNRPA Proteins) chromatin-remodeling complex, an essential event in Alpl (show ALPL Proteins) induction.
while p107 alone did not have an essential role in islet homeostasis, when combined with Rb deletion, its absence potentiated apoptosis of both alpha and beta cells resulting in glucose intolerance and diminished islet mass with ageing
Findings indicate that retinoblastoma-like protein p107 expression in stem cells commits cells to the white versus brown adipose lineage.
p107 retinoblastoma protein is regulated by Cdk6 (show CDK6 Proteins)/Ccnd1 (show CCND1 Proteins) in growth plates.
results reveal an overlapping role for pRB (show PGR Proteins) and p107 in cartilage development, endochondral ossification and enchondroma formation that reflects their coordination of cell-cycle exit at appropriate developmental stages
Rb, p107 and p130 epigenetically protect newly born cortical neurons from DNA damage and cell division
Data show that p21Cip1 (show CDKN1A Proteins) inactivation increases proliferation in Rb/p107DKO retina
The protein encoded by this gene is similar in sequence and possibly function to the product of the retinoblastoma 1 (RB1) gene. The RB1 gene product is a tumor suppressor protein that appears to be involved in cell cycle regulation, as it is phosphorylated in the S to M phase transition and is dephosphorylated in the G1 phase of the cell cycle. Both the RB1 protein and the product of this gene can form a complex with adenovirus E1A protein and SV40 large T-antigen, with the SV40 large T-antigen binding only to the unphosphorylated form of each protein. In addition, both proteins can inhibit the transcription of cell cycle genes containing E2F binding sites in their promoters. Due to the sequence and biochemical similarities with the RB1 protein, it is thought that the protein encoded by this gene may also be a tumor suppressor. Two transcript variants encoding different isoforms have been found for this gene.
retinoblastoma-like 1 (p107)
, retinoblastoma-like protein 1
, retinoblastoma-like protein 1-like
, 107 kDa retinoblastoma-associated protein
, cellular protein 107