Phospho-RB1 (S807) Recombinant Monoclonal Antibody

The DNA encoding for the human monoclonal antibody against the synthetic phosphopeptide of RB1 (S807) was integrated into the plasmid and subsequently transfected into the cell line for in vitro expression. After purification from the tissue culture supernatant (TCS) through affinity-chromatography, the recombinant monoclonal phospho-RB1 (S807) antibody was isolated. This phospho-RB1 Ser807 antibody specifically detects endogenous RB1 protein only when phosphorylated at Serine 807. It is a rabbit IgG and is reactive with human samples. This antibody is suitable for ELISA and IF analyses.

RB1 gene is the first isolated tumor suppressor gene in humans. It acts as a negative regulator of the cell cycle and regulates the expression of genes involved in cell proliferation and differentiation by binding with the transcription factor E2F1, thus maintaining the equilibrium of cell growth and development. Therefore, the function of the RB1 gene is intricately linked to the cell cycle, cell senescence, cell apoptosis, cell differentiation, and growth inhibition. Generally, Rb1 phosphorylation is crucial for releasing transcriptional target inhibition and facilitating cell cycle progression.

RB1 is a tumor suppressor that plays a critical role in regulating the G1/S transition of the cell cycle. The hypophosphorylated form of RB1 binds to transcription regulators of the E2F family, preventing the transcription of E2F-responsive genes. RB1 physically blocks the transactivating domain of E2Fs and recruits chromatin-modifying enzymes that actively repress transcription. Cyclin and CDK-dependent phosphorylation of RB1 leads to its dissociation from E2Fs, thereby activating the transcription of E2F responsive genes and initiating entry into the S phase. RB1 also promotes the G0-G1 transition upon phosphorylation and activation by CDK3/cyclin-C.

RB1 is directly involved in heterochromatin formation by maintaining the overall chromatin structure, particularly that of constitutive heterochromatin, through stabilization of histone methylation. It recruits and targets histone methyltransferases SUV39H1, KMT5B and KMT5C, resulting in epigenetic transcriptional repression. RB1 controls histone H4 'Lys-20' trimethylation and inhibits the intrinsic kinase activity of TAF1. Furthermore, it mediates transcriptional repression by SMARCA4/BRG1 by recruiting a histone deacetylase (HDAC) complex to the c-FOS promoter. In resting neurons, transcription of the c-FOS promoter is inhibited by BRG1-dependent recruitment of a phospho-RB1-HDAC1 repressor complex. Upon calcium influx, RB1 is dephosphorylated by calcineurin, leading to the release of the repressor complex.

In the context of viral infections, interactions with SV40 large T antigen, HPV E7 protein, or adenovirus E1A protein induce the disassembly of the RB1-E2F1 complex, disrupting RB1's activity.

1. Concurrent mutations in genes such as CDKN2B or RB1 were associated with worse clinical outcomes in lung adenocarcinoma patients with EGFR active mutations. PMID: 29343775
2. Mutational screening of the germline RB1 gene in Vietnamese patients with retinoblastoma revealed three novel mutations. PMID: 29568217
3. Analyses with phospho-defective and phospho-mimetic mutants of FoxM1b identified a critical role of the Plk1 phosphorylation sites in regulating the binding of FoxM1b to Rb and DNMT3b. PMID: 28387346
4. The accumulation of sequence variations in the RB1 gene might influence Greek patients' susceptibility towards the progression of cervical neoplasia. PMID: 30303478
5. Vitiligo lesions exhibited dysregulated SUMOylation and deSUMOylation in keratinocytes. Dysregulation of cell cycle progression was observed in SUMO1 knockdown HaCaT cells, and the deSUMOylation of Rb in keratinocytes may play a significant role in the development of vitiligo. PMID: 30066925
6. The Rb1 tumor suppressor gene modifies telomeric chromatin architecture by regulating TERRA expression. PMID: 28169375
7. These findings demonstrate that developmental stage-specific, as well as species- and cell type-specific features, sensitize to RB1 inactivation and reveal the human cone precursors' capacity to model retinoblastoma initiation, proliferation, premalignant arrest, and tumor growth. PMID: 30213853
8. Low pRB expression is associated with mouth cancer. PMID: 30275188
9. Control of the Restriction Point by Rb and p21. PMID: 30111539
10. Results showed that a) alterations of the p53 and Rb pathways are associated with high proliferation of tumor cells in BUC and b) high expression of cell-cycle proteins is associated with adverse histopathological parameters of these tumors. PMID: 29970521
11. The present result indicated that vascular smooth proliferation is regulated by activation of the NF-kappaB p65/miR17/RB pathway. As NF-kappaB p65 signaling is activated in and is a master regulator of the inflammatory response, the present findings may provide a mechanism for the excessive proliferation of VSMCs under inflammation during vascular disorders and may identify novel targets for the treatment of vascular d... PMID: 29115381
12. Reduced RB expression in medullary thyroid cancer is associated with decreased patient survival in univariate and multivariable analyses, independent from patient age at surgery or advanced TNM stage. PMID: 29105562
13. According to immunohistochemistry and immunoblot analysis, the expression levels of cyclin D1, cyclin E, pRb, and Ki67 in psoriasis lesions decreased after treatment and were similar to those in the normal group. PMID: 29115643
14. Data indicate that nuclear envelope rupture in cancer cells is likely due to the loss of either the Rb or the p53 pathway. PMID: 28811362
15. Altered pRb is frequently expressed in gastric carcinoma, inversely correlates with tumor invasion and tumor stage, suggesting an early event in gastric carcinogenesis. PMID: 28965621
16. Results define a network of E2F target genes susceptible to the regulatory influence of H1.2, where H1.2 augments global association of pRb with chromatin, enhances transcriptional repression by pRb, and facilitates pRb-dependent cell-cycle arrest. PMID: 28614707
17. The increased expression of miR-503-5p significantly reduced the expressions of E2F transcription factor 3 (E2F3) mRNA and retinoblastoma protein (Rb)/E2F signaling pathway mRNA in bladder cancer cells. PMID: 29169421
18. Loss of Rb immunolabeling and KRAS mutation are promising molecular markers of the therapeutic response to platinum-based chemotherapy for pancreatic neuroendocrine neoplasm grade-3 (PanNEN-G3), and Rb for neuroendocrine tumor with G3 (NET-G3). PMID: 28455360
19. We recommend intensive ocular screening for patients with germline RB1 mutations for retinoblastoma as well as neuroimaging for pineoblastoma surveillance. There is an approximately 20% risk of developing second primary cancers among individuals with hereditary RB, higher among those who received radiotherapy for their primary RB tumors. PMID: 28674118
20. The SNPs rs 216311, rs 1800383 and rs 1800386 associated significantly with bleeding in study subjects. rs1800386 occurred in all with bleeding history, no ethnic variations were noted. PMID: 28091443
21. miR-215 promoted cell migration and invasion of gastric cancer by directly targeting RB1. PMID: 28689850
22. MiR-661 promotes metastasis of non-small cell lung cancer through RB/E2F1 signaling and epithelial-mesenchymal transition events. PMID: 28716024
23. RB1 was identified as a direct and functional target of miR-215. RB1 is generally down-regulated in glioma tissues and its expression inversely correlated with miR-215, which is up-regulated in high-grade glioma tissues, and its expression was negatively correlated with miR-215. PMID: 28573541
24. Loss of retinoblastoma in pleomorphic fibroma: An immunohistochemical and genomic analysis. PMID: 28543636
25. Results show that RB1 expression is regulated by cdc37 which facilitates its phosphorylation through increasing CDK4 stability. PMID: 29288563
26. SOX2 overexpression and the loss of Rb1 protein expression might have a pivotal role in the divergent differentiation of pluripotent embryonic-like epithelial cells and the development of esophageal small-cell carcinoma. PMID: 28106103
27. Several RB1 alterations associated with retinoblastoma in humans were present in several non-human primates without an apparent pathological effect. PMID: 28401291
28. Results suggest that RB1 is the dominant tumor suppressor PP in MCC, and that inactivation of RB1 by MCPyV-LT is largely sufficient for its growth-supporting function in established MCPyV-positive MCC cells. PMID: 27121059
29. The frequency and association of polymorphisms in the TP53 and RB1 genes with clinical characteristics in a group of children with retinoblastoma (RB) in northern Mexico, was examined. PMID: 28210099
30. RB underexpression is associated with tumor cell invasiveness and neuroendocrine differentiation in prostate cancer. PMID: 27015368
31. Authors show that MYC inhibition by Omomyc, a dominant-negative MYC, suppresses the growth of SCLC cells with TP53 and RB1 inactivation carrying MYC, MYCL, or MYCN amplification. PMID: 27105536
32. Data suggest that the platelet-derived growth factor receptor alpha (PDGFRalpha)/Stat3 transcription factor/Rb1 protein regulatory axis might represent a potential therapeutic target for glioblastoma (GBM) treatment. PMID: 27344175
33. miR-590 inhibits RB1 and promotes proliferation and invasion of T-cell acute lymphoblastic leukaemia cells. PMID: 27036041
34. Causative RB1 mutations in most bilateral retinoblastoma (RB) patients and in some unilateral RB patients, including five novel mutations, were identified. PMID: 29261756
35. Homozygous loss of RB1 is an independent prognostic marker in multiple myeloma. PMID: 28234347
36. In certain contexts, Rb loss enables TRbeta1-dependent suppression of SKP2 as a safeguard against RB1-deficient tumorigenesis. TRbeta2 counteracts TRbeta1, thus disrupting this safeguard and promoting the development of RB1-deficient malignancies. PMID: 28972075
37. Expression levels of miR-675-5p in glioma tissues and cells were negatively correlated with RB1 expression at both mRNA and protein levels and promoted cell proliferation and migration. PMID: 28970140
38. Disruption of DREAM and RB-E2F complexes by oncoproteins from DNA tumor viruses leads to upregulation of cell cycle genes and impairs growth-inhibiting pathways, including the p53-mediated downregulation of cell cycle genes. [review] PMID: 28799433
39. A relatively stable genome in retinoblastoma tumor cells is maintained by TRb1 and TRb2-mediated PTTG1 inhibition, counteracting Rb-deficiency-related genomic instability. PMID: 28242412
40. APC/C and pRB interact with each other via the co-activator of APC/C, FZR1, providing an alternative pathway of regulation of G1 to S transition by pRB using a post-translational mechanism. Both pRB and FZR1 have complex roles and are implicated not only in regulation of cell proliferation but also in differentiation, quiescence, apoptosis, maintenance of chromosomal integrity, and metabolism. PMID: 27402801
41. Analysis of the spectrum of RB1 variants observed in 60,706 exomes identifies 197 variants that have enough potential to disrupt splicing to warrant further consideration. PMID: 28780672
42. AR also indirectly increases the expression of DNA replication genes through stimulatory effects on other metabolic genes with subsequent CDK activation and Rb hyperphosphorylation. PMID: 27760327
43. Rb gene promoter methylation was more frequent in gastric cancer patients than in controls. PMID: 28319413
44. We report the significance of genetic testing in the early detection and management of retinoblastoma from India. PMID: 26914665
45. Results show that the functional state of protein Rb is inferred to be inactive due to its phosphorylation status in the MYCN-amplified retinoblastoma without coding sequence mutations. This makes inactivation of RB1 by gene mutation or by protein phosphorylation, a necessary condition for initiating retinoblastoma tumorigenesis, independent of MYCN amplification. PMID: 28211617
46. Low RB expression is associated with osteosarcoma. PMID: 28655788
47. Loss of RB1 is associated with papillomavirus involvement in Barrett's dysplasia and esophageal adenocarcinoma. PMID: 28722212
48. The epigenetic interaction between Linc00441 and bidirectional transcripted neighbor RB1 may be a de novo theory cutting-point for the inactivation of RB1 in HCC. PMID: 28300839
49. The data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression. PMID: 28973440
50. RB inactivation enhances pro-inflammatory signaling through stimulation of the interleukin-6/STAT3 pathway, which directly promotes various malignant features of cancer cells. [review] PMID: 28865172

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HGNC: 9884

OMIM: 109800

KEGG: hsa:5925

STRING: 9606.ENSP00000267163

UniGene: Hs.408528