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Recombinant Human Charged multivesicular body protein 4b (CHMP4B)

ACP03158

Number
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Specifications


Cat.No ACP03158 Target NameCHMP4B
FormLiquid or Lyophilized powderExpression SystemE.coli
Expression Range1-224aaMol Weight51.8kDa
Protein LengthFull lengthPurityGreater than 90% as determined by SDS-PAGE.
Storage Buffer5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0.

Immunogen Information


Target SpeciesHumanUniprot IDQ9H444
Background Information
  • Uniprot Id

    Q9H444

  • Target Species

    Human

  • Target Name

    CHMP4B

  • Target Full Name

    Charged multivesicular body protein 4b

  • Target 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. Together with SPAST, the ESCRT-III complex promotes nuclear envelope sealing and mitotic spindle disassembly during late anaphase. Plays a role in the endosomal sorting pathway. ESCRT-III proteins are believed to mediate the necessary vesicle extrusion and/or membrane fission activities, possibly in conjunction with the AAA ATPase VPS4. When overexpressed, membrane-assembled circular arrays of CHMP4B filaments can promote or stabilize negative curvature and outward budding. CHMP4A/B/C are required for the exosomal release of SDCBP, CD63 and syndecan.; (Microbial infection) The ESCRT machinery also functions in topologically equivalent membrane fission events, such as the budding of enveloped viruses (HIV-1 and other lentiviruses). Via its interaction with PDCD6IP involved in HIV-1 p6- and p9-dependent virus release.

  • Target Involvement

    Cataract 31, multiple types (CTRCT31)

  • Target Subcellular Location

    Cytoplasm, cytosol. Late endosome membrane; Peripheral membrane protein. Midbody. Nucleus envelope.

  • Target Protein Families

    SNF7 family

  • Target Tissue Specificity

    Widely expressed. Expressed at higher level in heart and skeletal muscle. Also expressed in brain, colon, thymus, spleen, kidney, liver, small intestine, placenta, lung and peripheral blood lymphocytes.

  • Target Research Area

    others

  • Target Synonyms

    Charged multivesicular body protein 4b; CHM4B_HUMAN; chmp4b; Chromatin-modifying protein 4b; hSnf7-2; hVps32-2; SNF7 homolog associated with Alix 1; SNF7-2; Vacuolar protein sorting-associated protein 32-2; Vps32-2

  • Target Background

    This gene encodes a member of the chromatin-modifying protein/charged multivesicular body protein (CHMP) protein family. The protein is part of the endosomal sorting complex required for transport (ESCRT) complex III (ESCRT-III), which functions in the sorting of endocytosed cell-surface receptors into multivesicular endosomes. The ESCRT machinery also functions in the final abscisson stage of cytokinesis and in the budding of enveloped viruses such as HIV-1. The three proteins of the CHMP4 subfamily interact with programmed cell death 6 interacting protein (PDCD6IP, also known as ALIX), which also functions in the ESCRT pathway. The CHMP4 proteins assemble into membrane-attached 5-nm filaments that form circular scaffolds and promote or stabilize outward budding. These polymers are proposed to help generate the luminal vesicles of multivesicular bodies. Mutations in this gene result in autosomal dominant posterior polar cataracts.

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