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1 to 13 of 13  Show
  1. 1
    Cited for: NUCLEOTIDE SEQUENCE.
    Category: Sequences.
    Tissue: Amygdala.
    Source: UniProtKB/TrEMBL (unreviewed).
  2. 2
    "The chaperone environment at the cytoplasmic face of the endoplasmic reticulum can modulate rhodopsin processing and inclusion formation."
    Chapple J.P., Cheetham M.E.
    J. Biol. Chem. 278:19087-19094(2003) [PubMed] [Europe PMC] [Abstract]
    Category: Subcellular Location, Interaction.
    Annotation: data provide evidence that cytoplasmic chaperones HSJ1a and HSJ1b when targeted to the endoplasmic reticulum can influence the folding and processing of rhodopsin.
    Source: GeneRIF:3300.

    This publication is mapped to 8 other entries.

  3. 3
    "HSJ1 is a neuronal shuttling factor for the sorting of chaperone clients to the proteasome."
    Westhoff B., Chapple J.P., van der Spuy J., Hoehfeld J., Cheetham M.E.
    Curr. Biol. 15:1058-1064(2005) [PubMed] [Europe PMC] [Abstract]
    Category: Function.
    Annotation: HSJ1 is a neuronal shuttling factor for the sorting of chaperone clients to the proteasome.
    Source: GeneRIF:3300.

    This publication is cited by 2 and mapped to 2 other entries.

  4. 4
    Category: Function.
    Annotation: Cystamine and cysteamine increase brain levels of BDNF in Huntington disease via HSJ1b and transglutaminase.
    Source: GeneRIF:3300.

    This publication is mapped to 25 other entries.

  5. 5
    "A genetic association analysis of cognitive ability and cognitive ageing using 325 markers for 109 genes associated with oxidative stress or cognition."
    Harris S.E., Fox H., Wright A.F., Hayward C., Starr J.M., Whalley L.J., Deary I.J.
    BMC Genet. 8:43-43(2007) [PubMed] [Europe PMC] [Abstract]
    Category: Function, Pathology & Biotech, Sequences.
    Annotation: Observational study of gene-disease association. (HuGE Navigator). [GeneRIF:3300]. Not Associated with NEUROLOGICAL: cognitive trait. [GAD:581308].
    Source: GeneRIF:3300, GAD:581308.

    This publication is mapped to 686 other entries.

  6. 6
    "Gene expression profiling in human skeletal muscle during recovery from eccentric exercise."
    Mahoney D.J., Safdar A., Parise G., Melov S., Fu M., MacNeil L., Kaczor J., Payne E.T., Tarnopolsky M.A.
    Am. J. Physiol. Regul. Integr. Comp. Physiol. 294:R1901-10(2008) [PubMed] [Europe PMC] [Abstract]
    Category: Expression.
    Annotation: Damaging exercise induced the expression of capZalpha MCIP1 CARP1 DNAJB2 c-myc and junD each of which are likely involved in skeletal muscle growth remodeling and stress management.
    Source: GeneRIF:3300.

    This publication is mapped to 79 other entries.

  7. 7
    "Oxidative stress, telomere length and biomarkers of physical aging in a cohort aged 79 years from the 1932 Scottish Mental Survey."
    Starr J.M., Shiels P.G., Harris S.E., Pattie A., Pearce M.S., Relton C.L., Deary I.J.
    Mech. Ageing Dev. 129:745-751(2008) [PubMed] [Europe PMC] [Abstract]
    Category: Function, Pathology & Biotech.
    Annotation: Observational study of gene-disease association. (HuGE Navigator). [GeneRIF:3300]. Not Associated with AGING: Aging/ Telomere Length. [GAD:581307].
    Source: GeneRIF:3300, GAD:581307.

    This publication is mapped to 692 other entries.

  8. 8
    Category: Expression, Sequences.
    Annotation: Data show that DNAJB2 is expressed in skeletal muscle at the neuromuscular junction of normal fibers in the cytoplasm and membrane of regenerating fibers and in protein aggregates and vacuoles in protein aggregate myopathies.
    Source: GeneRIF:3300.

    This publication is mapped to 23 other entries.

  9. 9
    Category: Sequences.
    Annotation: a mutation causing a loss-of-function of HSJ1 is linked to a pure lower motor neuron disease strongly suggesting that HSJ1 also plays an important and specific role in motor neurons.
    Source: GeneRIF:3300.

    This publication is mapped to 2 other entries.

  10. 10
    "Molecular chaperone mediated late-stage neuroprotection in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis."
    Novoselov S.S., Mustill W.J., Gray A.L., Dick J.R., Kanuga N., Kalmar B., Greensmith L., Cheetham M.E.
    PLoS ONE 8:E73944-E73944(2013) [PubMed] [Europe PMC] [Abstract]
    Category: Function, Pathology & Biotech.
    Annotation: HSJ1a acts on mutant SOD1 through a combination of chaperone co-chaperone and pro-ubiquitylation activity.
    Source: GeneRIF:3300.

    This publication is mapped to 15 other entries.

  11. 11
    "HSJ1-related hereditary neuropathies: novel mutations and extended clinical spectrum."
    Gess B., Auer-Grumbach M., Schirmacher A., Strom T., Zitzelsberger M., Rudnik-Schoneborn S., Rohr D., Halfter H., Young P., Senderek J.
    Neurology 83:1726-1732(2014) [PubMed] [Europe PMC] [Abstract]
    Category: Sequences.
    Annotation: The results of this study confirm that HSJ1 mutations are a rare but detectable cause of autosomal recessive dHMN and CMT2.
    Source: GeneRIF:3300.

    This publication is mapped to 2 other entries.

  12. 12
    "Identification of a Large DNAJB2 Deletion in a Family with Spinal Muscular Atrophy and Parkinsonism."
    Sanchez E., Darvish H., Mesias R., Taghavi S., Firouzabadi S.G., Walker R.H., Tafakhori A., Paisan-Ruiz C.
    Hum. Mutat. 37:1180-1189(2016) [PubMed] [Europe PMC] [Abstract]
    Category: Function.
    Annotation: Study describes the identi fi cation of the fi rst deletion reported at the DNAJB2 locus further expanding its phenotypic and genotypic spectrums as well as its disease-associated mechanisms with spinal muscular atrophy and parkinsonism.
    Source: GeneRIF:3300.

    This publication is mapped to 3 other entries.

  13. 13
    "Protein kinase CK2 modulates HSJ1 function through phosphorylation of the UIM2 domain."
    Ottaviani D., Marin O., Arrigoni G., Franchin C., Vilardell J., Sandre M., Li W., Parfitt D.A., Pinna L.A., Cheetham M.E., Ruzzene M.
    Hum. Mol. Genet. 26:611-623(2017) [PubMed] [Europe PMC] [Abstract]
    Category: Function.
    Annotation: Our results disclose a novel interplay between ubiquitin- and phosphorylation-dependent signalling and represent the first report of a regulatory mechanism for UIM-dependent function. They also suggest that CK2 inhibitors could release the full neuroprotective potential of HSJ1 and deserve future interest as therapeutic strategies for neurodegenerative disease.
    Source: GeneRIF:3300.

    This publication is mapped to 8 other entries.

1 to 13 of 13  Show
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