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Mouse Anti-CHMP2B Recombinant Antibody (CBXC-0417) (CBMAB-C5894-CQ)

This product is a mouse antibody that recognizes CHMP2B. The antibody CBXC-0417 can be used for immunoassay techniques such as: ELISA.
See all CHMP2B antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBXC-0417
Antibody Isotype
IgG1, κ
Application
ELISA

Basic Information

Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.2
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Charged Multivesicular Body Protein 2B
Introduction
This gene encodes a component of the heteromeric ESCRT-III complex (Endosomal Sorting Complex Required for Transport III) that functions in the recycling or degradation of cell surface receptors. ESCRT-III functions in the concentration and invagination of ubiquitinated endosomal cargos into intralumenal vesicles. The protein encoded by this gene is found as a monomer in the cytosol or as an oligomer in ESCRT-III complexes on endosomal membranes. It is expressed in neurons of all major regions of the brain. Mutations in this gene result in one form of familial frontotemporal lobar degeneration.
Entrez Gene ID
25978
UniProt ID
Q9UQN3
Alternative Names
Charged Multivesicular Body Protein 2B; Chromatin Modifying Protein 2B; CHMP2.5; VPS2-2; Vacuolar Protein-Sorting-Associated Protein 2-2; Vacuolar Protein Sorting-Associated Protein 2-2; VPS2 Homolog B (S. Cerevisiae); Chromatin-Modifying Protein 2b;
Function
Probable core component of the endosomal sorting required for transport complex III (ESCRT-III) which is involved in multivesicular bodies (MVBs) formation and sorting of endosomal cargo proteins into MVBs. MVBs contain intraluminal vesicles (ILVs) that are generated by invagination and scission from the limiting membrane of the endosome and mostly are delivered to lysosomes enabling degradation of membrane proteins, such as stimulated growth factor receptors, lysosomal enzymes and lipids. The MVB pathway appears to require the sequential function of ESCRT-O, -I,-II and -III complexes. ESCRT-III proteins mostly dissociate from the invaginating membrane before the ILV is released. The ESCRT machinery also functions in topologically equivalent membrane fission events, such as the terminal stages of cytokinesis and the budding of enveloped viruses (HIV-1 and other lentiviruses). ESCRT-III proteins are believed to mediate the necessary vesicle extrusion and/or membrane fission activities, possibly in conjunction with the AAA ATPase VPS4.
Biological Process
Autophagy Source: ParkinsonsUK-UCL
Cognition Source: UniProtKB
Endosomal transport Source: Reactome
Endosome organization Source: UniProtKB
Endosome transport via multivesicular body sorting pathway Source: GO_Central
ESCRT III complex disassembly Source: ParkinsonsUK-UCL
Late endosome to vacuole transport Source: GO_Central
Macroautophagy Source: ParkinsonsUK-UCL
Midbody abscission Source: UniProtKB
Mitotic metaphase plate congression Source: UniProtKB
Mitotic nuclear envelope reassembly Source: Reactome
Multivesicular body assembly Source: ParkinsonsUK-UCL
Multivesicular body-lysosome fusion Source: ParkinsonsUK-UCL
Neuron cellular homeostasis Source: UniProtKB
Nucleus organization Source: UniProtKB
Positive regulation of viral release from host cell Source: UniProtKB
Protein transport Source: GO_Central
Regulation of centrosome duplication Source: UniProtKB
Regulation of mitotic spindle assembly Source: UniProtKB
Viral budding via host ESCRT complex Source: UniProtKB
Viral life cycle Source: Reactome
Cellular Location
Late endosome membrane; Cytosol
Involvement in disease
Frontotemporal dementia and/or amyotrophic lateral sclerosis 7 (FTDALS7): A neurodegenerative disorder characterized by frontotemporal dementia and/or amyotrophic lateral sclerosis in affected individuals. There is high intrafamilial variation. Frontotemporal dementia (FTD) is characterized by frontal and temporal lobe atrophy associated with neuronal loss, gliosis, and dementia. Patients exhibit progressive changes in social, behavioral, and/or language function. Amyotrophic lateral sclerosis (ALS) is characterized by the death of motor neurons in the brain, brainstem, and spinal cord, resulting in fatal paralysis. FTDALS7 is an autosomal dominant form characterized by onset of ALS or FTD in adulthood. A few patients may have both phenotypes.

Li, T., Yin, Y., Mu, N., Wang, Y., Liu, M., Chen, M., ... & Ma, H. (2021). Metformin-Enhanced Cardiac AMP-Activated Protein Kinase/Atrogin-1 Pathways Inhibit Charged Multivesicular Body Protein 2B Accumulation in Ischemia–Reperfusion Injury. Frontiers in Cell and Developmental Biology, 1865.

Alqabandi, M., de Franceschi, N., Maity, S., Miguet, N., Bally, M., Roos, W. H., ... & Mangenot, S. (2021). The ESCRT-III isoforms CHMP2A and CHMP2B display different effects on membranes upon polymerization. BMC biology, 19(1), 1-18.

Ugbode, C., & West, R. J. (2021). Lessons learned from CHMP2B, implications for frontotemporal dementia and amyotrophic lateral sclerosis. Neurobiology of disease, 147, 105144.

Gupta, N., Sahar, T., Khowal, S., Ganaie, I. A., Mughees, M., Khullar, D., ... & Wajid, S. (2021). Differential levels of CHMP2B, LLPH, and SLC25A51 proteins in secondary renal amyloidosis. Expert Review of Proteomics, 18(1), 65-73.

Li, T., Yin, Y., Mu, N., Wang, Y., Liu, M., Chen, M., ... & Ma, H. (2020). Metformin-Enhanced Cardiac AMP-Activated Protein Kinase/Atrogin-1 Pathways Inhibit Charged Multivesicular Body Protein 2B Accumulation in Ischemia–Reperfusion Injury. Frontiers in cell and developmental biology, 8.

Lu, Y., West, R. J., Pons, M., Sweeney, S. T., & Gao, F. B. (2020). Ik2/TBK1 and Hook/Dynein, an adaptor complex for early endosome transport, are genetic modifiers of FTD-associated mutant CHMP2B toxicity in Drosophila. Scientific reports, 10(1), 1-10.

Midani-Kurçak, J. S., Dinekov, M., Puladi, B., Arzberger, T., & Köhler, C. (2019). Effect of tau-pathology on charged multivesicular body protein 2b (CHMP2B). Brain research, 1706, 224-236.

Wilson, C. M. (2018). Human Charged Multivesicular Body Protein 2B (CHMP2B) Mutant Variant CHMP2BIntron5 Causes Notch Signaling Gain-of-Function Phenotypes in Drosophila External Sense Organ Cell Lineages.

Zhang, Y., Schmid, B., Nikolaisen, N. K., Rasmussen, M. A., Aldana, B. I., Agger, M., ... & FReJA Consortium. (2017). Patient iPSC-derived neurons for disease modeling of frontotemporal dementia with mutation in CHMP2B. Stem cell reports, 8(3), 648-658.

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For research use only. Not intended for any clinical use.

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