関: casein kinase I

WordNet

look over, usually with the intention to rob; "They men cased the housed"
the quantity contained in a case (同)caseful
a specific state of mind that is temporary; "a case of the jitters"
(printing) the receptacle in which a compositor has his type, which is divided into compartments for the different letters, spaces, or numbers; "for English, a compositor will ordinarily have two such cases, the upper case containing the capitals and the lower case containing the small letters" (同)compositor''s case, typesetter''s case
a glass container used to store and display items in a shop or museum or home (同)display case, showcase, vitrine
bed linen consisting of a cover for a pillow; "the burglar carried his loot in a pillowcase" (同)pillowcase, slip, pillow slip
a portable container for carrying several objects; "the musicians left their instrument cases backstage"
nouns or pronouns or adjectives (often marked by inflection) related in some way to other words in a sentence (同)grammatical case
an occurrence of something; "it was a case of bad judgment"; "another instance occurred yesterday"; "but there is always the famous example of the Smiths" (同)instance, example
a person requiring professional services; "a typical case was the suburban housewife described by a marriage counselor"
a problem requiring investigation; "Perry Mason solved the case of the missing heir"
a statement of facts and reasons used to support an argument; "he stated his case clearly"
the actual state of things; "that was not the case"
a milk protein used in making e.g. plastics and adhesives
an enzyme that catalyzes the conversion of a proenzyme to an active enzyme
the basic unit of money in Papua New Guinea

PrepTutorEJDIC

〈C〉(…の)『実例』,事例《+『of』+『名』》 / 《the case》『実情』,真相 / 〈C〉〈U〉『場合』,情況,事情,立場 / 〈C〉(…の)(決定すべき)問題,重大事《+『of』+『名』》 / 〈C〉『訴訟』[『事件』],裁判 / 〈C〉(正当な)論拠,弁護;(被告または原告の)主張,申し立て / 〈C〉病状,容態;(症状から見た)患者 / 〈C〉〈U〉格(名詞・代名詞の語形変化)
(運搬・保管用のいろいろな)『箱』,ケース / (各種の)『容器』,筒,さや,袋,おおい / (標本・陳列用の)ガラス箱,戸だな / (戸・窓などの)わく / 活字箱 / …'を'箱(袋,さやなど)に入れる《+『名』+『up,』+『名』+『up』》
カゼイン,乾酪素(牛乳の蛋白質;絵具・接着剤にも用いる)

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English Journal

A novel mechanism of keratin cytoskeleton organization through casein kinase Iα and FAM83H in colorectal cancer.

Kuga T, Kume H, Kawasaki N, Sato M, Adachi J, Shiromizu T, Hoshino I, Nishimori T, Matsubara H, Tomonaga T.Author information Laboratory of Proteome Research, National Institute of Biomedical Innovation, Ibaraki, Osakai 567-0085, Japan.AbstractKeratin filaments form cytoskeletal networks in epithelial cells. Dynamic rearrangement of keratin filament networks is required for epithelial cells to perform cellular processes such as cell migration and polarization; however, the mechanism governing keratin filament rearrangement remains unclear. Here, we describe a novel mechanism of keratin cytoskeleton organization mediated by casein kinase Iα (CK-1α) and a newly identified keratin-associated protein, FAM83H. Knockdown of FAM83H induces keratin filament bundling, whereas overexpression of FAM83H disassembles keratin filaments, suggesting that FAM83H regulates the filamentous state of keratins. Intriguingly, keratin filament bundling is concomitant with the dissociation of CK-1α from keratin filaments, whereas aberrant speckle-like localization of CK-1α is observed concomitantly with keratin filament disassembly. Furthermore, CK-1α inhibition, similar to FAM83H knockdown, causes keratin filament bundling and reverses keratin filament disassembly induced by FAM83H overexpression, suggesting that CK-1α mediates FAM83H-dependent reorganization of keratin filaments. Because the N-terminal region of FAM83H interacts with CK-1α and the C-terminal region interacts with keratins, FAM83H might tether CK-1α to keratins. Colorectal cancer tissue also shows keratin filament disassembly accompanied with FAM83H overexpression and aberrant CK-1α localization, and FAM83H-overexpressing cancer cells exhibit loss or alteration of epithelial cell polarity. Importantly, knockdown of FAM83H inhibits cell migration accompanied by keratin cytoskeleton rearrangement in colorectal cancer cells. These results suggest that keratin cytoskeleton organization is regulated by FAM83H-mediated recruitment of CK-1α to keratins, and that keratin filament disassembly caused by overexpression of FAM83H and aberrant localization of CK-1α could contribute to the progression of colorectal cancer.
Journal of cell science.J Cell Sci.2013 Oct 15;126(Pt 20):4721-31. doi: 10.1242/jcs.129684. Epub 2013 Jul 31.
Keratin filaments form cytoskeletal networks in epithelial cells. Dynamic rearrangement of keratin filament networks is required for epithelial cells to perform cellular processes such as cell migration and polarization; however, the mechanism governing keratin filament rearrangement remains unclear
PMID 23902688

Stochastic machines as a colocalization mechanism for scaffold protein function.

Xue B, Romero PR, Noutsou M, Maurice MM, Rüdiger SG, William AM Jr, Mizianty MJ, Kurgan L, Uversky VN, Dunker AK.Author information Department of Molecular Medicine, University of South Florida, Tampa, FL 33612, USA.AbstractThe axis inhibition (Axin) scaffold protein colocalizes β-catenin, casein kinase Iα, and glycogen synthetase kinase 3β by their binding to Axin's long intrinsically disordered region, thereby yielding structured domains with flexible linkers. This complex leads to the phosphorylation of β-catenin, marking it for destruction. Fusing proteins with flexible linkers vastly accelerates chemical interactions between them by their colocalization. Here we propose that the complex works by random movements of a "stochastic machine," not by coordinated conformational changes. This non-covalent, modular assembly process allows the various molecular machine components to be used in multiple processes.
FEBS letters.FEBS Lett.2013 Jun 5;587(11):1587-91. doi: 10.1016/j.febslet.2013.04.006. Epub 2013 Apr 18.
The axis inhibition (Axin) scaffold protein colocalizes β-catenin, casein kinase Iα, and glycogen synthetase kinase 3β by their binding to Axin's long intrinsically disordered region, thereby yielding structured domains with flexible linkers. This complex leads to the phosphorylation of β-cateni
PMID 23603389

Casein kinase 1α regulates an MDMX intramolecular interaction to stimulate p53 binding.

Wu S, Chen L, Becker A, Schonbrunn E, Chen J.Author information Molecular Oncology Department, Moffitt Cancer Center, Tampa, Florida, USA.AbstractMDMX is an important regulator of p53 during embryonic development and malignant transformation. Previous studies showed that casein kinase 1α (CK1α) stably associates with MDMX, stimulates MDMX-p53 binding, and cooperates with MDMX to inactivate p53. However, the mechanism by which CK1α stimulates MDMX-p53 interaction remains unknown. Here, we present evidence that p53 binding by the MDMX N-terminal domain is inhibited by the central acidic region through an intramolecular interaction that competes for the p53 binding pocket. CK1α binding to the MDMX central domain and phosphorylation of S289 disrupts the intramolecular interaction, allowing the N terminus to bind p53 with increased affinity. After DNA damage, the MDMX-CK1α complex is disrupted by Chk2-mediated phosphorylation of MDMX at S367, leading to reduced MDMX-p53 binding. Therefore, CK1α is an important functional partner of MDMX. DNA damage activates p53 in part by disrupting CK1α-MDMX interaction and reducing MDMX-p53 binding affinity.
Molecular and cellular biology.Mol Cell Biol.2012 Dec;32(23):4821-32. doi: 10.1128/MCB.00851-12. Epub 2012 Oct 1.
MDMX is an important regulator of p53 during embryonic development and malignant transformation. Previous studies showed that casein kinase 1α (CK1α) stably associates with MDMX, stimulates MDMX-p53 binding, and cooperates with MDMX to inactivate p53. However, the mechanism by which CK1α stimulat
PMID 23028042