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anti-Human p107 Antibodies:
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Human Monoclonal p107 Primary Antibody for IP, WB - ABIN967438
Beijersbergen, Hijmans, Zhu, Bernards: Interaction of c-Myc with the pRb-related protein p107 results in inhibition of c-Myc-mediated transactivation. in The EMBO journal 1994
Show all 10 Pubmed References
Human Polyclonal p107 Primary Antibody for WB - ABIN1881732
Jayadeva, Kurimchak, Garriga, Sotillo, Davis, Haines, Mumby, Graña: B55alpha PP2A holoenzymes modulate the phosphorylation status of the retinoblastoma-related protein p107 and its activation. in The Journal of biological chemistry 2010
Show all 3 Pubmed References
Human Polyclonal p107 Primary Antibody for IP, IHC - ABIN333827
Tur, Etschmann, Benz, Leich, Waller, Schuh, Rosenwald, Ertl, Kienitz, Haaf, Bräuninger, Gattenlöhner: The 140-kD isoform of CD56 (NCAM1) directs the molecular pathogenesis of ischemic cardiomyopathy. in The American journal of pathology 2013
The authors found that phosphorylation of residues S650 and S975 in p107 weakens the E2F4 (show E2F4 Antibodies) transactivation domain binding.
UL97 phosphorylates and inactivates the retinoblastoma protein-related p107 and p130 (show RBL2 Antibodies) proteins
Sequence analysis of the RB1 (show RB1 Antibodies) gene detected a novel mutation in bilateral retinoblastoma.
MAGE (show MAGEB10 Antibodies)-A11 is a proto-oncogene (show RAB1A Antibodies) 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 Antibodies) and E2F1 (show E2F1 Antibodies).
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 Antibodies) gene in unilateral retinoblastoma.
identification of a PP2A (show PPP2R4 Antibodies) trimeric holoenzyme containing B55alpha (show PPP2R2A Antibodies), 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 Antibodies), p107 and E2F-4 (show E2F4 Antibodies) in human cells
suggests that the p107 N-terminus provides an interaction domain for transcription factors involved in cell cycle control
report shows hypophosphorylation of the retinoblastoma family proteins induced by H2O2 was because of the activity of protein phosphatase 2A
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 Antibodies) protein (Socs3 (show SOCS3 Antibodies)) expression in triple knockout (TKO (show MRPS12 Antibodies)) HSCs.
p107 is required for the efficient recruitment of an activating SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) chromatin-remodeling complex, an essential event in Alpl (show ALPL Antibodies) 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 Antibodies)/Ccnd1 (show CCND1 Antibodies) in growth plates.
results reveal an overlapping role for pRB (show PGR Antibodies) 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 Antibodies) inactivation increases proliferation in Rb/p107DKO retina
Mutation of p107 or p130 reduces survival of Rb-deficient myoblasts during differentiation.
Data show that p107-deficient muscle expresses increased levels of peroxisome proliferator-activated receptor gamma co-activator-1alpha and contains increased numbers of the pro-oxidative type I and type IIa myofibers.
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