Falcon deep research report for DNAJA2
Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Large-scale proteomics and phosphoproteomics of urinary exosomes.
The diverse members of the mammalian HSP70 machine show distinct chaperone-like activities.
Optimal functional levels of activation-induced deaminase specifically require the Hsp40 DnaJa1.
Binding of human nucleotide exchange factors to heat shock protein 70 (Hsp70) generates functionally distinct complexes in vitro.
A quantitative chaperone interaction network reveals the architecture of cellular protein homeostasis pathways.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Human CPR (cell cycle progression restoration) genes impart a Far- phenotype on yeast cells.
STIP1(HOP) binds HSP90 and HSP70:HSP40:nascent protein
HSP70 binds to HSP40:nascent protein
The self-association equilibrium of DNAJA2 regulates its interaction with unfolded substrate proteins and with Hsc70.
-
DNAJA2 reversibly self-assembles into highly ordered tubular oligomers (~200 angstrom width, D5 symmetry disks of five dimers) that can dissociate into active dimers; heat shock at 40 degrees C promotes dissociation with t1/2 ~2.3 min.
-
The intrinsically disordered C-terminal tail (V361-Q412) regulates holding activity and productive Hsc70 interaction.
-
Hsc70 drives DNAJA2 oligomer disassembly in an ATP-dependent manner via J-domain engagement.
Hsp70 and DNAJA2 limit CFTR levels through degradation.
-
DNAJA2 overexpression reduces CFTR maturation, consistent with increased ERAD of immature CFTR, in a J-domain-dependent manner.
-
DNAJA2 acts with Hsc70/Hsp70 and the E3 ubiquitin ligase CHIP to promote CFTR degradation at the ER.
DNAJA2 deficiency activates cGAS-STING pathway via the induction of aberrant mitosis and chromosome instability.
-
DNAJA2 localizes to centrosomes and promotes CMA-dependent degradation of PCM1 and CEP290 via Hsc70/LAMP2A.
-
Loss of DNAJA2 causes abnormal mitosis (~50% abnormal spindles), chromosome instability, and micronuclei formation activating cGAS-STING innate immunity.
Heat shock protein DNAJA2 regulates transcription-coupled repair by triggering CSB degradation via chaperone-mediated autophagy.
Hsp40s play complementary roles in the prevention of tau amyloid formation.
-
DNAJA2 potently suppresses tau amyloid formation using at least two binding sites; CTDI recognizes monomeric tau while CTDII binds aggregation-prone species and mature fibrils.
-
At sub-stoichiometric DNAJA2:tau ratios (0.5:1), 88% reduction in fibril mass was observed.
Mapping interactions with the chaperone network reveals factors that protect against tau aggregation.
Definition of pRb- and p53-dependent and -independent steps in HIRA/ASF1a-mediated formation of senescence-associated heterochromatin foci.
Regulation of p53 and cancer signaling by heat shock protein 40/J-domain protein family members.