Polyubiquitin-C is a protein encoded by the UBC gene in humans. [5] [6] [7] Polyubiquitin-C is one of the sources of ubiquitin, along with UBB, UBA52, and RPS27A. [8]
UBC gene is one of the two stress-regulated polyubiquitin genes (UBB and UBC) in mammals. It plays a key role in maintaining cellular ubiquitin levels under stress conditions. [9] [10] Defects of UBC gene could lead to mid-gestation embryonic lethality.
UBC gene is located at chromosome 12q24.3, consisting of 2 exons. The promoter of the UBC gene contains putative heat shock elements ( HSEs), which mediates UBC induction upon stress. UBC gene differs from UBB gene in the number of Ub coding units they contain. [9] Nine to ten Ub units were in the UBC gene.
In polyubiquitin-C, the C-terminus of a given ubiquitin molecule is covalently conjugated to either the N-terminal residue or one of seven lysine residues of another ubiquitin molecule. [11] Different linking of ubiquitin chains results in distinct conformations. There are 8 linkage types of polyubiquitin-C, and each type possesses the linkage-dependent dynamics and a linkage-specific conformation. [12] [13]
The diversity of polyubiquitin-C means that ubiquitylation contributes to the regulation of many cellular events. Polyubiquitin-C doesn’t activate the heat-shock response, but it plays a key role in sustaining the response. UBC gene transcription is induced during stress and provides extra ubiquitin necessary to remove damaged/unfolded proteins. [10] [14] Polyubiquitin-C has important role in diverse biological processes, such as innate immunity, DNA repair and kinase activity. [15] [16] [17] Unanchored polyubiquitin-C are also key signaling molecules that connect and coordinate the proteasome and autophagy to eliminate toxic protein aggregates. [18]
Loss of a single UBC allele has no apparent phenotype, while homozygous deletion of UBC gene leads to mid-gestation embryonic lethality due to a defect in fetal liver development, as well as a delay in cell-cycle progression and increased susceptibility to cellular stress. [10] It is also reported that homozygous deletion of UBC gene in mouse embryonic fibroblasts will cause decreased cellular Ub level and reduced viability under oxidative stress. [19]
Polyubiquitin-C has been shown to interact with:
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Aliases | UBC, HMG20, Ubiquitin C | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 191340; MGI: 98889; HomoloGene: 128418; GeneCards: UBC; OMA: UBC - orthologs | ||||||||||||||||||||||||||||||||||||||||||||||||||
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Polyubiquitin-C is a protein encoded by the UBC gene in humans. [5] [6] [7] Polyubiquitin-C is one of the sources of ubiquitin, along with UBB, UBA52, and RPS27A. [8]
UBC gene is one of the two stress-regulated polyubiquitin genes (UBB and UBC) in mammals. It plays a key role in maintaining cellular ubiquitin levels under stress conditions. [9] [10] Defects of UBC gene could lead to mid-gestation embryonic lethality.
UBC gene is located at chromosome 12q24.3, consisting of 2 exons. The promoter of the UBC gene contains putative heat shock elements ( HSEs), which mediates UBC induction upon stress. UBC gene differs from UBB gene in the number of Ub coding units they contain. [9] Nine to ten Ub units were in the UBC gene.
In polyubiquitin-C, the C-terminus of a given ubiquitin molecule is covalently conjugated to either the N-terminal residue or one of seven lysine residues of another ubiquitin molecule. [11] Different linking of ubiquitin chains results in distinct conformations. There are 8 linkage types of polyubiquitin-C, and each type possesses the linkage-dependent dynamics and a linkage-specific conformation. [12] [13]
The diversity of polyubiquitin-C means that ubiquitylation contributes to the regulation of many cellular events. Polyubiquitin-C doesn’t activate the heat-shock response, but it plays a key role in sustaining the response. UBC gene transcription is induced during stress and provides extra ubiquitin necessary to remove damaged/unfolded proteins. [10] [14] Polyubiquitin-C has important role in diverse biological processes, such as innate immunity, DNA repair and kinase activity. [15] [16] [17] Unanchored polyubiquitin-C are also key signaling molecules that connect and coordinate the proteasome and autophagy to eliminate toxic protein aggregates. [18]
Loss of a single UBC allele has no apparent phenotype, while homozygous deletion of UBC gene leads to mid-gestation embryonic lethality due to a defect in fetal liver development, as well as a delay in cell-cycle progression and increased susceptibility to cellular stress. [10] It is also reported that homozygous deletion of UBC gene in mouse embryonic fibroblasts will cause decreased cellular Ub level and reduced viability under oxidative stress. [19]
Polyubiquitin-C has been shown to interact with: