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anti-Human DNAJC5 Antikörper:
anti-Mouse (Murine) DNAJC5 Antikörper:
anti-Rat (Rattus) DNAJC5 Antikörper:
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Human Polyclonal DNAJC5 Primary Antibody für ICC, IP - ABIN1742330
García-Junco-Clemente, Cantero, Gómez-Sánchez, Linares-Clemente, Martínez-López, Luján, Fernández-Chacón: Cysteine string protein-alpha prevents activity-dependent degeneration in GABAergic synapses. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
Show all 5 Pubmed References
This review summarizes studies that elucidate the neuroprotective role of Drosophila CSP, which is critical for maintaining neurotransmitter release and preventing neurodegeneration.
these data suggest that CSP promotes synaptic growth and evoked neurotransmitter release by mechanistically independent signaling pathways
study found dHIP14 to be an essential maternal effect (zeige NLRP5 Antikörper) gene required for photoreceptor synaptic transmission and for proper in vivo expression of the palmitoylated presynaptic proteins SNAP-25 (zeige SNAP25 Antikörper) and cysteine string protein
Our data indicate that HIP14 (zeige ZDHHC17 Antikörper) controls neurotransmitter release by regulating the trafficking of CSP to synapses.
csp interaction with Hsc 70 (zeige HSPA8 Antikörper) molecular chaperones is vital for regulated secretion in Xenopus oocytes
The importance of specific residues in the cysteine-string domain was investigated, revealing that a central core of palmitoylated cysteines is essential for aggregation of adult-onset neuronal ceroid lipofuscinosis (zeige CLN6 Antikörper) CSPalpha L115R/L116 mutants.
Phosphorylation of CSP triggers a major conformational switch that modulates its protein interactions.
In fact, DnaJC5 overexpression induced tau release in cells, neurons, and brain tissue, but only when activity of the chaperone Hsc70 (zeige HSPA8 Antikörper) was intact and when tau was able to associate with this chaperone.
This study demonstrated that Neuronal ceroid lipofuscinosis with DNAJC5/CSPalpha mutation has PPT1 pathology and exhibit aberrant protein palmitoylation.
Missense mutations in DNAJC5 does not play a major role in PD in the Chinese population.
Results indicate of a p.L116del mutation in DNAJC5 from families with autosomal dominant Kufs disease.
Palmitoylation-induced aggregation of mutant CSP-alpha proteins may underlie the development of adult-onset neuronal ceroid lipofuscinosis (zeige CLN6 Antikörper)
association of DNAJC5 mutations with autosomal dominant Kufs disease
This is the first replication study of the identification of DNAJC5 as the disease-causing gene for autosomal dominant ANCL. The identification of the novel gene in ANCL will allow us to gain a better understanding of the pathological mechanism of ANCLs
First evidence that CSP and HSP70 (zeige HSP70 Antikörper), and their interactions with MARCKS (zeige MARCKS Antikörper), are involved in mucin (zeige SLC13A2 Antikörper) secretion from airway epithelium.
These data show that neurodegenerative processes associated with lysosomal dysfunction may be presynaptically initiated by a concomitant reduction in alpha-synuclein and CSPalpha levels at nerve terminals.
The mRNA and protein expression of CSP1 (zeige RCAN1 Antikörper) was elevated in 3T3-L1 adipocytes in insulin (zeige INS Antikörper) resistant states caused by high levels of palmitate and chronic insulin (zeige INS Antikörper) exposure.
gamma-Synuclein binds synaptic vesicles but is unable to rescue the phenotype of CSPalpha-deficient mice.
Using hippocampal cultures, study shows that CSPalpha regulates the stability of client proteins and synaptic vesicle number. Analysis of CSPalpha-dynamin 1 (zeige DNM1 Antikörper) interactions reveals unexpectedly that CSPalpha regulates the polymerization of dynamin 1 (zeige DNM1 Antikörper).
Study shows that cysteine string protein-alpha is required to maintain the size of the releasable pool of synaptic vesicles in motorneurons, presumably by conveying stability to SNAP-25 (zeige SNAP25 Antikörper).
findings suggest that the neurodegeneration in CSPalpha KO mice is primarily produced by defective SNAP-25 (zeige SNAP25 Antikörper) function, which causes neurodegeneration by impairing SNARE (zeige VTI1B Antikörper)-complex assembly
Data indicate that Cspalpha interacts with Syt9 (zeige SYT9 Antikörper), and such a complex may be relevant in the calcium-mediated control of a late stage of exocytosis by triggering the specific recruitment of a folding catalyst at the fusion point.
Data show that deletion of CSPalpha produces an abnormal SNAP-25 (zeige SNAP25 Antikörper) conformer that inhibits SNARE (zeige VTI1B Antikörper)-complex formation, and is subject to ubiquitylation and proteasomal degradation.
CSPalpha is not essential for the normal operation of Ca2 (zeige CA2 Antikörper)+ channels or exocytosis but acts as a presynaptic chaperone that maintains continued synaptic function. Its deletion causes postnatal lethality of knockout mice.
Tonically active ribbon synapses in retina are particularly sensitive to the deletion of CSPalpha and that expression of at least one CSP isoform is essential to protect such tonically active synapses from neurodegeneration.
This gene is a member of the J protein family. J proteins function in many cellular processes by regulating the ATPase activity of 70 kDa heat shock proteins. The encoded protein plays a role in membrane trafficking and protein folding, and has been shown to have anti-neurodegenerative properties. The encoded protein is known to play a role in cystic fibrosis and Huntington's disease. A pseudogene of this gene is located on the short arm of chromosome 8.
, cystein string protein
, cysteine string protein
, cysteine string protein 3
, cysteine-string protein
, DnaJ (Hsp40) homolog, subfamily C, member 5
, cysteine string protein alpha
, dnaJ homolog subfamily C member 5