Ask about this productRelated genes to: RAP1B Blocking Peptide
- Gene:
- RAP1B NIH gene
- Name:
- RAP1B, member of RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- K-REV, RAL1B, DKFZp586H0723
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
Related products to: RAP1B Blocking Peptide
Related articles to: RAP1B Blocking Peptide
- The inhibited migration of dendritic cells (DCs) from lesion tissue to draining lymph nodes is a possible way for tumors to achieve immune evasion. In a previous study, we demonstrated that high concentrations of Prostaglandin E2 (PGE), which were expressed in tumor microenvironments, inhibited DCs' migration. However, the specific mechanism is not yet clear. The current study aims to use the murine bone marrow-derived DCs (BMDCs) to demonstrate the possible signaling pathway of PGE. The mRNA and protein expressions of the Epac1-Rap1 axis and PKA-CREB axis were determined after administration of PGE on DCs. Then, the agonist and antagonist of these molecules were used to treat DCs. The migration capability of DCs was detected as well as the RhoA activation levels. The mRNA and protein of Epac1 were barely undetectable in DCs. The use of Epac1 agonists showed no impact on DCs' migration capability and RhoA activation levels. The activation levels of Rap1 and protein expressions of Rap1a and Rap1b were not affected by PGE administration. The using of Rap1a and Rap1b antagonists demonstrated no impact on DCs' migration capability and RhoA activation levels. Moreover, the PKA activation levels and phosphorylated CREB1 were increased by the administration of PGE on DCs. The application of a PKA inhibitor attenuated the effect of PGE in a 3D migration assay and in vivo experiment. These results suggest that the PKA-CREB axis, instead of Epac1-Rap1, probably associates with the intracellular signaling pathway induced by high PGE levels, which demonstrates an inhibitory effect on DCs' migration. These findings can bring a different perspective on immunological surveillance of tumor progression. - Source: PubMed
Publication date: 2026/05/14
Diao GeHuang JieTian MinLi RunboGuo JianxinHan Jian - Chicken coccidiosis inflicts severe economic losses on the poultry industry. The mechanisms underlying Eimeria tenella (E. tenella) invasion, colonization, and damage to host cells remain incompletely elucidated. This study was designed to elucidate EtMIC2-interacting proteins and the mechanism that EtMIC2 regulates E. tenella invasion and host cell apoptosis. His pull-down-MS and KEGG enrichment results showed apoptosis-related proteins including ITGAV (Integrin alpha-V), PlexinB2, MAP2K6, GNA11, TRK, CASP7, PAK1, and RAP1b. Only the interaction model between EtMIC2 and ITGAV met the AlphaFold2 thresholds (pLDDT > 70, pTM+ipTM > 0.75). The CO-IP results showed that in the primary host cells (CECs) of E. tenella, protein bands corresponding to EtMIC2 (50 kDa) and ITGAV (135 kDa) were successfully detected in the IP group. Blue colony growth on SD/-Ade,-His,-Leu,-Trp/X-α-Gal plates for the group pGBKT7-EtMIC2 or pGBKT7-EtMIC2-3 (153-1029 bp) or pGBKT7-EtMIC2-5 (855-1029 bp) co-transformed with pGADT7-ITGAV in Yeast Two-Hybrid assay. Green fluorescence was observed in DF-1 cells pBiFC-EtMIC2-VN173 or pBiFC-EtMIC2-3-VN173 or pBiFC-EtMIC2-5-VN173 were co-transfected with pBiFC-ITGAV-VC155 in Bimolecular fluorescence complementation. The addition of EtMIC2 protein significantly increased (P < 0.05) E. tenella infection rate, gene expression and protein activity of ITGAV, FAK, PLC, PKC, p65, PI3K, Akt, ERK, and Bcl2, and reduced host cell Caspase 3 activity, apoptosis rate, gene expression and protein activity of JNK, p38, Bax, and Caspase 3. Knockdown of ITGAV produced the opposite effects. The function of EtMIC2 was prevented following the knockdown of ITGAV. The above finding indicate that the EtMIC2 855-1029 bp (285-342 aa) region interacts with ITGAV, leading to the upregulation of ITGAV, FAK, PLC, PKC, p65, PI3K, Akt, ERK, and Bcl2, while downregulating JNK, p38, Bax, and Caspase 3, thereby promoting E. tenella invasion and inhibiting host cell apoptosis. - Source: PubMed
Publication date: 2026/04/09
Cui Kai-LingGuo Lu-LuLei XuanChen Ying-YingLiu Kui-HaoDuan Bu-TingZhang Hong-HuiLv Xiao-LingZheng Ming-Xue - This research investigates miR-28-5p in type 2 diabetes mellitus (T2DM), aiming to clarify its mechanistic role and clinical significance in the pathogenesis of diabetic retinopathy (DR). - Source: PubMed
Publication date: 2026/04/22
Li JunliZhou YijunWei LichunZhao YanWu MinLi Chunjian - Distinct effector-binding preferences among RAS family GTPases challenge the longstanding view that canonical RAS proteins uniformly bind and activate RAF, PI3Kα, RalGDS, and other downstream effectors. Quantitative binding data, supported by structural insights into effector recognition, instead reveal a division of labor: the canonical RAS subfamily (KRAS, HRAS, NRAS) binds RAF kinases with high affinity, the RRAS subfamily (RRAS2 and MRAS) preferentially engages PI3Kα, and the RAP subfamily (RAP1A and RAP1B) shows the strongest binding to RalGDS. These intrinsic preferences, encoded in the switch regions and further shaped by isoform and effector expression, as well as subcellular localization, establish a hierarchy in which canonical RAS, RRAS2/MRAS, and RAP1A/B primarily activate RAF, PI3Kα, and RalGDS, respectively, in normal cells. Oncogenic mutations at codons G12, G13, or Q61 disrupt this hierarchy by driving sustained accumulation of GTP-bound canonical RAS, enabling engagement of lower-affinity effectors such as PI3Kα and RalGDS. In addition, certain mutations, including KRAS-G12D and -G12V, modestly enhance PI3Kα binding, representing a neomorphic expansion of effector engagement. Together, these effects bypass intrinsic effector selectivity, allowing canonical RAS to co-opt effectors normally associated with other RAS subfamilies and broaden downstream signaling. This framework explains how inherent effector preferences govern normal signaling and how oncogenic mutations override these constraints to expand effector engagement in RAS-driven cancers. - Source: PubMed
Simanshu Dhirendra KMcCormick Frank - A detailed description of prenatal ultrasound signs of congenital renal cystic dysplasia (CRCD) is reported. Molecular investigations identified the c.179G>T, p.(Gly60Val) "de novo" variant in a heterozygous state in the RAP1B gene. This is a missense variant not described in the literature. Predictive tools suggest a pathogenic role for this mutation and a likely association with the clinical phenotype. - Source: PubMed
Publication date: 2026/03/13
Cordisco AdalgisaMagliulo StefaniaDi Marco ChiaraFortuna ElisaTerracciano AlessandraMeloni Claudio