Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Chandana Kondapalli"'
Autor:
Annie Lee, Chandana Kondapalli, Daniel M. Virga, Tommy L. Lewis, So Yeon Koo, Archana Ashok, Georges Mairet-Coello, Sebastien Herzig, Marc Foretz, Benoit Viollet, Reuben Shaw, Andrew Sproul, Franck Polleux
Publikováno v:
Nature Communications, Vol 13, Iss 1, Pp 1-20 (2022)
Loss of excitatory synapses occur prior to the formation of amyloid plaques in Alzheimer’s disease. Here the authors show in an animal model that the loss of synapses induced by amyloid-beta oligomers requires over-activation of a stress-response p
Externí odkaz:
https://doaj.org/article/e4cca8864343441c862cd2169b11e9ee
Autor:
Chandana Kondapalli, Agne Kazlauskaite, Ning Zhang, Helen I. Woodroof, David G. Campbell, Robert Gourlay, Lynn Burchell, Helen Walden, Thomas J. Macartney, Maria Deak, Axel Knebel, Dario R. Alessi, Miratul M. K. Muqit
Publikováno v:
Open Biology, Vol 2, Iss 5 (2012)
Summary Missense mutations in PTEN-induced kinase 1 (PINK1) cause autosomal-recessive inherited Parkinson's disease (PD). We have exploited our recent discovery that recombinant insect PINK1 is catalytically active to test whether PINK1 directly phos
Externí odkaz:
https://doaj.org/article/a7ccab88220e49e2ad360b217db36be0
Autor:
Annie Lee, Chandana Kondapalli, Daniel M. Virga, Tommy L. Lewis, So Yeon Koo, Archana Ashok, Georges Mairet-Coello, Sebastien Herzig, Marc Foretz, Benoit Viollet, Reuben Shaw, Andrew Sproul, Franck Polleux
Publikováno v:
Nature Communications
Nature Communications, 2022, 13 (1), pp.4444. ⟨10.1038/s41467-022-32130-5⟩
Nature Communications, 2022, 13 (1), pp.4444. ⟨10.1038/s41467-022-32130-5⟩
During the early stages of Alzheimer’s disease (AD) in both mouse models and human patients, soluble forms of Amyloid-β 1–42 oligomers (Aβ42o) trigger loss of excitatory synapses (synaptotoxicity) in cortical and hippocampal pyramidal neurons (
Autor:
Sébastien Herzig, Annie Lee, Georges Mairet-Coello, Chandana Kondapalli, Reuben J. Shaw, Tommy L. Lewis, Archana Ashok, Daniel M. Virga, Franck Polleux, Koo Sy, Andrew Sproul
During the early stages of Alzheimer’s disease (AD) in both mouse models and human patients, soluble forms of Amyloid-β1-42 oligomers (Aβ42o) trigger loss of excitatory synapses (synaptotoxicity) in cortical and hippocampal pyramidal neurons (PNs
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d8200e45beeb032b4903d257a23f6c74
https://doi.org/10.1101/637199
https://doi.org/10.1101/637199
Autor:
Helen I. Woodroof, Matthias Trost, Miratul M. K. Muqit, Chandana Kondapalli, Brian D. Dill, Robert Gourlay, James B. Procter, Aymelt Itzen, Yu-Chiang Lai, Mark Peggie, Olga Corti, Ronny Lehneck, David G. Campbell, Thomas Macartney, Jean-Christophe Corvol
Publikováno v:
The EMBO Journal
EMBO Journal
EMBO Journal, EMBO Press, 2015, 34 (22), pp.2840-2861. 〈10.15252/embj.201591593〉
EMBO Journal, 2015, 34 (22), pp.2840-2861. ⟨10.15252/embj.201591593⟩
EMBO Journal, EMBO Press, 2015, 34 (22), pp.2840-2861. ⟨10.15252/embj.201591593⟩
EMBO Journal
EMBO Journal, EMBO Press, 2015, 34 (22), pp.2840-2861. 〈10.15252/embj.201591593〉
EMBO Journal, 2015, 34 (22), pp.2840-2861. ⟨10.15252/embj.201591593⟩
EMBO Journal, EMBO Press, 2015, 34 (22), pp.2840-2861. ⟨10.15252/embj.201591593⟩
International audience; Mutations in the PTEN-induced kinase 1 (PINK1) are causative of autosomal recessive Parkinson's disease (PD). We have previously reported that PINK1 is activated by mitochondrial depolarisation and phosphorylates serine 65 (Se
Autor:
Agne, Kazlauskaite, Chandana, Kondapalli, Robert, Gourlay, David G, Campbell, Maria Stella, Ritorto, Kay, Hofmann, Dario R, Alessi, Axel, Knebel, Matthias, Trost, Miratul M K, Muqit
Publikováno v:
Biochemical Journal
We have previously reported that the Parkinson's disease-associated kinase PINK1 (PTEN-induced putative kinase 1) is activated by mitochondrial depolarization and stimulates the Parkin E3 ligase by phosphorylating Ser65 within its Ubl (ubiquitin-like
Publikováno v:
Journal of Biological Chemistry. 284:27135-27145
Receptor guanylyl cyclases are multidomain proteins, and ligand binding to the extracellular domain increases the levels of intracellular cGMP. The intracellular domain of these receptors is composed of a kinase homology domain (KHD), a linker of ∼
Autor:
David G. Campbell, Maria Deak, Helen I. Woodroof, Dario R. Alessi, Robert Gourlay, Ning Zhang, Miratul M. K. Muqit, Agne Kazlauskaite, Helen Walden, Axel Knebel, Thomas Macartney, Chandana Kondapalli, Lynn Burchell
Publikováno v:
Open Biology
Open Biology, Vol 2, Iss 5 (2012)
Open Biology, Vol 2, Iss 5 (2012)
Summary Missense mutations in PTEN-induced kinase 1 (PINK1) cause autosomal-recessive inherited Parkinson's disease (PD). We have exploited our recent discovery that recombinant insect PINK1 is catalytically active to test whether PINK1 directly phos
Autor:
Sayanti, Saha, Kabir Hassan, Biswas, Chandana, Kondapalli, Nishitha, Isloor, Sandhya S, Visweswariah
Publikováno v:
The Journal of biological chemistry. 284(40)
Receptor guanylyl cyclases are multidomain proteins, and ligand binding to the extracellular domain increases the levels of intracellular cGMP. The intracellular domain of these receptors is composed of a kinase homology domain (KHD), a linker of app
Autor:
Matthias Trost, Axel Knebel, Chandana Kondapalli, Miratul M. K. Muqit, Kay Hofmann, Ritorto, Alessi, David G. Campbell, Agne Kazlauskaite, Robert Gourlay
Publikováno v:
Journal of Neurology, Neurosurgery & Psychiatry. 85:e4.148-e4
Mutations in the PINK1 and Parkin genes are associated with autosomal-recessive Parkinson9s disease. PINK1 encodes a mitochondrial localized protein kinase and Parkin encodes an ubiquitin E3 ligase. Several lines of evidence indicate that the enzymes