Yoko Nekooki-Machida
Overview
Explore the profile of Yoko Nekooki-Machida including associated specialties, affiliations and a list of published articles.
Author names and details appear as published. Due to indexing inconsistencies, multiple individuals may share a name, and a single author may have variations. MedLuna displays this data as publicly available, without modification or verification
Snapshot
Snapshot
Articles
11
Citations
250
Followers
0
Related Specialties
Related Specialties
Top 10 Co-Authors
Top 10 Co-Authors
Published In
Affiliations
Affiliations
Soon will be listed here.
Recent Articles
1.
Nakakura T, Suzuki T, Horiguchi K, Tanaka H, Arisawa K, Miyashita T, et al.
Cell Tissue Res
. 2021 Jan;
384(2):449-463.
PMID: 33447878
Endothelial fenestrae are the transcellular pores existing on the capillary walls which are organized in clusters referred to as sieve plates. They are also divided by a diaphragm consisting of...
2.
Nakakura T, Suzuki T, Tanaka H, Arisawa K, Miyashita T, Nekooki-Machida Y, et al.
Cell Tissue Res
. 2020 Sep;
383(2):823-833.
PMID: 32910242
Endothelial fenestrae are transcellular pores that pierce the capillary walls in endocrine glands such as the pituitary. The fenestrae are covered with a thin fibrous diaphragm consisting of the plasmalemma...
3.
Nekooki-Machida Y, Hagiwara H
Med Mol Morphol
. 2020 Jul;
53(4):191-197.
PMID: 32632910
Acetylation is a well-studied post-translational modification (PTM) of tubulin. Acetylated tubulin is present in the centrioles, primary cilia, and flagella, which contain long-lived stable microtubules. Tubulin acetylation plays an important...
4.
Hui K, Takashima N, Watanabe A, Chater T, Matsukawa H, Nekooki-Machida Y, et al.
Sci Adv
. 2019 Apr;
5(4):eaau8237.
PMID: 30989111
Dysfunctional mTOR signaling is associated with the pathogenesis of neurodevelopmental and neuropsychiatric disorders. However, it is unclear what molecular mechanisms and pathogenic mediators are involved and whether mTOR-regulated autophagy continues...
5.
Nekooki-Machida Y, Nakakura T, Nishijima Y, Tanaka H, Arisawa K, Kiuchi Y, et al.
Med Mol Morphol
. 2018 Jun;
51(4):217-226.
PMID: 29869029
Acetylation of α-tubulin is a well-studied posttranscriptional modification, which is mostly catalyzed by α-tubulin N-acetyltransferase (ATAT1). ATAT1 possibly affects various cellular functions related with microtubules, such as intracellular transport, cell...
6.
Endo R, Takashima N, Nekooki-Machida Y, Komi Y, Hui K, Takao M, et al.
Biol Psychiatry
. 2018 May;
84(7):509-521.
PMID: 29752072
Background: Neurodegenerative diseases involving protein aggregation often accompany psychiatric symptoms. Frontotemporal lobar degeneration (FTLD) associated with TAR DNA-binding protein 43 (TDP-43) aggregation is characterized by progressive neuronal atrophy in frontal...
7.
Nakakura T, Suzuki T, Torii S, Asano-Hoshino A, Nekooki-Machida Y, Tanaka H, et al.
Cell Tissue Res
. 2017 Jul;
370(1):169-178.
PMID: 28687926
The production and secretion of adrenocorticotropin, a proopiomelanocortin (POMC)-derived hormone, by corticotrophs in the anterior pituitary, is regulated by corticotrophin-releasing hormone (CRH) and glucocorticoids. We have previously demonstrated that adrenalectomy...
8.
Tanaka M, Ishizuka K, Nekooki-Machida Y, Endo R, Takashima N, Sasaki H, et al.
J Clin Invest
. 2017 Mar;
127(4):1438-1450.
PMID: 28263187
Huntington's disease (HD) is a polyglutamine (polyQ) disease caused by aberrant expansion of the polyQ tract in Huntingtin (HTT). While motor impairment mediated by polyQ-expanded HTT has been intensively studied,...
9.
Nakakura T, Suzuki T, Horiguchi K, Fujiwara K, Tsukada T, Asano-Hoshino A, et al.
Med Mol Morphol
. 2016 Sep;
50(2):59-67.
PMID: 27660208
S100β-positive cells exist in the marginal cell layer (MCL) of the adenohypophysis and follicle structure in the parenchyma of anterior lobe (ALFS) in pituitary. They have multiple functions as phagocytes...
10.
Tonoki A, Kuranaga E, Ito N, Nekooki-Machida Y, Tanaka M, Miura M
Genes Cells
. 2011 Apr;
16(5):557-64.
PMID: 21466635
Polyglutamine diseases, including Machado-Joseph disease and Huntington's disease, typically appear in midlife and are characterized by amyloid accumulations of abnormally expanded polyglutamine proteins. Although there is growing evidence that aging...