Ask about this productRelated genes to: DNAJA2 antibody
- Gene:
- DNAJA2 NIH gene
- Name:
- DnaJ heat shock protein family (Hsp40) member A2
- Previous symbol:
- -
- Synonyms:
- HIRIP4, DNAJ, CPR3, DNJ3
- Chromosome:
- 16q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-09
- Date modifiied:
- 2016-10-05
Related products to: DNAJA2 antibody
Related articles to: DNAJA2 antibody
- BACKGROUND: As a molecular chaperone of heat shock protein 70 (HSP70), DnaJ heat shock protein family member A2 (DNAJA2) can facilitate protein folding under stress conditions and has recently emerged as a novel and critical regulator that modulates the innate immune response. The V protein of Newcastle disease virus (NDV) is a crucial virulence factor; however, its relationship with the heat shock protein family remains poorly understood. RESULTS: We identified the interaction between DNAJA2 and NDV V proteins through immunoprecipitation‒mass spectrometry (IP‒MS) and confirmed that this interaction occurred mainly at residues 101–367 aa of DNAJA2. This finding was further validated by confocal microscopy and coimmunoprecipitation (co-IP). We found that the expression level of DNAJA2 is elevated during NDV infection. The overexpression of DNAJA2 enhances the expression of melanoma differentiation-associated gene 5 (MDA5) and mitochondrial antiviral signaling protein (MAVS), which upregulate the production of interferon-stimulated genes (ISGs) and interferon-β (IFN-β), thereby inhibiting the replication of NDV. In contrast, DNAJA2 knockdown promoted viral replication. CONCLUSIONS: Notably, DNAJA2-mediated modulation of innate immunity occurred specifically in the presence of NDV or NDV V proteins, suggesting that DNAJA2 potentially activates immune signaling pathways by targeting the NDV V protein. These findings establish the role of DNAJA2 against NDV and combine the heat shock protein family with the innate immune pathway, providing new institutional insights into the relationship between the virus and the host and the prevention and control of the virus. - Source: PubMed
Publication date: 2025/12/22
Mo JiacongZhang FanJiang YuLi MingrongWu ShutingChen Ruiai - Dysregulation of heat shock protein DNAJA2 induces genomic instability and was consequently hypothesized to promote tumorigenesis. However, DNAJA2 knockout mice do not develop cancer but exhibit neonatal lethality and the underlying mechanism remains unknown. Here, we demonstrate that DNAJA2 maintains homeostatic glucose metabolism by regulating insulin signaling. Mechanistically, DNAJA2 binds to the insulin receptor (IR) and prevents adaptor protein 2 (AP2)-mediated spontaneous IR endocytosis by inhibiting the IR-AP2 interaction. Thus, DNAJA2 defects lead to reduced IR localization on the plasma membrane and suppression of the insulin-stimulated signaling cascade, thereby inhibiting glycogen synthesis and storage in the liver during embryogenesis, further resulting in neonatal lethality of DNAJA2-deficient mice. Analysis of public datasets reveals a strong association between DNAJA2 and metabolic phenotypes, including type 2 diabetes mellitus (T2DM) and obesity, in both humans and mice. In conclusion, our study elucidates the mechanism by which DNAJA2 regulates IR endocytosis, insulin signaling and glucose metabolism, shedding light on the pathogenesis of metabolic disorders. - Source: PubMed
Publication date: 2025/11/13
Qin YuanhuaWu WenjunLin KequanDavis Anthony JHuang Yaping - In viral infections human heat shock proteins (HSPs) play a dual role by either protecting host cells or acting on viruses' needs. The roles of HSPs have been extensively studied in various human pathologies, but their involvement in the progression of COVID-19 remains unexplored. It makes HSPs genetic variants particularly interesting in the context of severe COVID-19 risk. In this study, 1228 subjects (199 hospitalized COVID-19 patients and 962 controls) were genotyped for 20 SNPs in genes encoding and their regulators. SNP rs7189628 (effect allele [EA] T) increased the risk of severe COVID-19 in the entire group ( = 0.002), males ( = 0.00008), and smokers ( = 0.0003). SNP rs910652 (EA C) decreased the risk of severe COVID-19 in the entire group ( = 0.01), females ( = 0.04), and patients with normal physical activity levels ( = 0.01). SNP rs1136141 (EA A) increased the risk of severe COVID-19 in patients with low fruit/vegetable intake ( = 0.004). Moreover, we observed significant changes in ground-glass opacity and alterations in blood coagulation and inflammation parameters, influenced by the SNPs of , , , , , and . The molecular mechanisms underlying these associations are discussed. Together, our study provides preliminary evidence that SNPs of HSPs can significantly modulate the risk of severe COVID-19. - Source: PubMed
Publication date: 2025/09/15
Karpenko Andrey RKobzeva Ksenia AOrlov Yuriy LBushueva Olga Yu - The chaperoning system, which is responsible for protein homeostasis, plays a significant role in cardiovascular diseases. Among molecular chaperones or heat shock proteins (HSPs), the HSP40 family, the main co-chaperone of HSP70, remains largely underexplored, especially in ischemic heart disease (IHD) risk. - Source: PubMed
Publication date: 2025/09/10
Polshvedkina OlgaKobzeva KseniaBushueva Olga - Sporadic Alzheimer's disease and some forms of frontotemporal lobar degeneration (FTLD-tau) are neurological disorders of later life where cognitive deficits follow from the progressive accumulation of microtubule-associated tau protein. Disease-related tau accumulation is marked by altered subcellular distribution and rearrangement of this natively unstructured protein into alternative conformational forms, including highly organized fibrillar assemblies. With a partial analogy to effects seen in prion diseases, pathological tau conformers have a templating activity called seeding that may be measured in cellular and cell-free systems. Moreover, cellular systems and disease models can recapitulate "strain effects" wherein the same tau amino acid sequence can adopt markedly different conformations. Here we analyzed FTLD-tau conformers in cellular reporter systems expressing a pro-aging mutant form of the lamin A protein termed "progerin." Measured versus the baseline performance of a reporter system based on HEK293 cells, the addition of tau burden or progerin expression produced only mild changes in proteomic analyses or morphology, whereas application of both stressors produced a notable shift in ER stress and homeostasis, including increased levels of DNAJC10 and DNAJA2. The phenotypic effects scored here appear unrelated to the generation of new tau strains or to the type of strain input, insofar as progerin-expressing cells were more responsive to tau seeding by diverse brain samples containing different populations of tau conformers. Thus, premature aging and disease-associated tau conformers can exhibit an additive relationship in a model system. - Source: PubMed
Publication date: 2025/07/15
Han Zhuang ZhuangKang Sang-GyunGomez-Cardona ErikWohlgemuth SereneShmeit KlintonArce LuisSafar Jiri GJulien OlivierWestaway David