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DnaJ heat shock protein family member C10 (DNAJC10)
- Target
- DNAJC10
- Molecular classification
- Enzyme, Protein-folding chaperone, Endoplasmic reticulum-associated degradation component (ERAD), Heat shock protein (Hsp40 family)
01
Overview
DnaJ heat shock protein family member C10 (DNAJC10) is an endoplasmic reticulum (ER) co-chaperone and disulfide reductase belonging to the Hsp40 family, with crucial functions in ER-associated degradation (ERAD) and protein quality control. It reduces non-native disulfide bonds in misfolded glycoproteins, facilitating their refolding or degradation, and interacts with ERAD components including EDEM and chaperones like HSPA5/GRP78. DNAJC10 is upregulated in certain cancers, particularly acute myeloid leukemia (AML), where it promotes leukemia stem cell (LSC) survival, ER homeostasis, and chemoresistance. Its inhibition triggers ER stress, activates the PERK-EIF2α-CHOP branch of the unfolded protein response, and induces apoptosis, making it a candidate therapeutic target for improving chemotherapy responses in AML.
- Other names
- DnaJ homolog subfamily C member 10ERDJ5UNQ495/PRO1012ER-resident protein ERdj5MTHrPDIA19Endoplasmic reticulum DNA J domain-containing protein 5MacrothioredoxinJPDIJ-domain-containing protein disulfide isomerase-like protein
02
Mechanism of action
Inhibitors or silencing of DNAJC10 induce ER stress and apoptosis by activating the PERK-EIF2α-ATF4 branch of the unfolded protein response (UPR) in leukemia; indirect sensitization to cytotoxic agents via pro-apoptotic pathway activation
03
Biological functions
Protein foldingProtein quality controlUbiquitin-proteasome system regulationEndoplasmic reticulum (ER) stress responseRegulation of apoptosis (context-dependent, notably in leukemia stem cells)
04
Disease associations
Cancer (notably acute myeloid leukemia, some solid tumors)Potential biomarker and therapeutic target in leukemiaOther roles reported in solid tumors and possible connection to maxillary cancer and cholera (associative)
05
Safety considerations
DNAJC10 is not required for normal hematopoiesis in mice, suggesting hematological tolerability, but broad role in ER proteostasis could present off-target toxicity or adverse effects if globally inhibitedSpecificity of action in different cancer types or tissues may affect therapeutic window—reported pro-apoptotic and anti-apoptotic roles depending on cellular context
06
Interacting drugs
Cytarabine (Ara-C) (sensitization described via target inhibition in AML context)
2 more in the full profile.
07
Biomarkers
Overexpression of DNAJC10 is a poor prognostic indicator in acute myeloid leukemiaGRP78 and GRP94 levels (ER stress markers elevated with DNAJC10 manipulation, especially in knockout or silencing models)
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