Key Specifications Table
|Species Reactivity||Key Applications|
|Presentation||Anti-IGF2BP2 (Mouse Monoclonal). One vial containing 12.5 µg protein G purified monoclonal in buffer containing 0.1 M Tris-glycine (pH 7.4), 150mM NaCl, 0.05% sodium azide before the addition of glycerol to 30%. Store at -20° C.
Concentration: 0.176 mg/mL
Normal mouse IgG. One vial containing 125 µg purified mouse IgG in 125 µL storage buffer containing 0.1% sodium azide. Store at -20°C.
RIP Primer IGF2. One vial containing 75 μL of 5 μM of each primer specific for human IGF2 mRNA. Store at -20°C.
FOR: GCG GCT TCT ACT TCA GCA G
REV: CAG GTG TCA TAT TGG AAG AAC
|Safety Information according to GHS|
|Material Size||10 assays|
|Material Package||10 assays per set. Recommended use: 1.25 μg of antibody per RIP (dependent upon biological context).|
RIPAb+™ IGF2BP2 Antibody SDS
|Monoclonal Antibody/Primer Set_2833939||2833939|
|RIPAb+ IGF2BP2 - Q1999625||Q1999625|
|RIPAb+ IGF2BP2 - 2559240||2559240|
|RIPAb+ IGF2BP2 - 3229614||3229614|
|RIPAb+ IGF2BP2 - 3506767||3506767|
|RIPAb+ IGF2BP2 - 3793160||3793160|
|RIPAb+ IGF2BP2 -2752496||2752496|
|RIPAb+ IGF2BP2 -2793776||2793776|
|Reference overview||Application||Pub Med ID|
|RNA-binding proteins regulate the expression of the immune activating ligand MICB.|
Nachmani, D; Gutschner, T; Reches, A; Diederichs, S; Mandelboim, O
Nature communications 5 4186 2014
The recognition of stress-induced ligands by the activating receptor NKG2D expressed on cytotoxic lymphocytes is crucial for the prevention and containment of various diseases and is also one of the best-studied examples of how danger is sensed by the immune system. Still, however, the mechanisms leading to the expression of the NKG2D ligands are far from being completely understood. Here, we use an unbiased and systematic RNA pull-down approach combined with mass spectrometry to identify six RNA-binding proteins (RBPs) that bind and regulate the expression of MICB, one of the major stress-induced ligands of NKG2D. We further demonstrate that at least two of the identified RBPs function during genotoxic stress. Our data provide insights into stress recognition and hopefully open new therapeutic venues.
|Oncogenic NRAS, required for pathogenesis of embryonic rhabdomyosarcoma, relies upon the HMGA2-IGF2BP2 pathway.|
Li, Z; Zhang, Y; Ramanujan, K; Ma, Y; Kirsch, DG; Glass, DJ
Cancer Res 73 3041-50 2013
Embryonic rhabdomyosarcoma (ERMS) is the most common soft-tissue tumor in children. Here, we report the identification of the minor groove DNA-binding factor high mobility group AT-hook 2 (HMGA2) as a driver of ERMS development. HMGA2 was highly expressed in normal myoblasts and ERMS cells, where its expression was essential to maintain cell proliferation, survival in vitro, and tumor outgrowth in vivo. Mechanistic investigations revealed that upregulation of the insulin-like growth factor (IGF) mRNA-binding protein IGF2BP2 was critical for HMGA2 action. In particular, IGF2BP2 was essential for mRNA and protein stability of NRAS, a frequently mutated gene in ERMS. shRNA-mediated attenuation of NRAS or pharmacologic inhibition of the MAP-ERK kinase (MEK)/extracellular signal-regulated kinase (ERK) effector pathway showed that NRAS and NRAS-mediated signaling was required for tumor maintenance. Taken together, these findings implicate the HMGA2-IGFBP2-NRAS signaling pathway as a critical oncogenic driver in ERMS.