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1 ubunits of the microtubule-severing complex, katanin.
2 ule severing enzymes, Spastin, Fidgetin, and Katanin.
3 axon lose their characteristic resistance to katanin.
4 related to the microtubule-severing protein katanin.
5 in vitro; thus, it is an ortholog of animal katanin.
6 centrosome-associated WD repeat protein p80-katanin.
7 y subunit of the microtubule-severing enzyme Katanin.
8 subunits of the microtubule-severing ATPase katanin.
9 altered with regard to their sensitivity to katanin.
10 5, and the microtubule-severing protein, p60/katanin.
11 which results in ubiquitin laddering of p60/katanin.
12 that regulate the severing properties of P60-katanin.
13 interacts with ciliary proteins and p60/p80 katanins.
16 as been observed in vitro to be catalyzed by katanin, a heterodimeric adenosine triphosphatase that c
18 equired after meiosis to negatively regulate katanin, a microtubule-severing complex, permitting the
21 plant cell wall since mutants with decreased katanin activity have been shown to have defective walls
22 zymes and suggest a scheme for regulation of katanin activity in cells dependent on free tubulin conc
27 itro data, whereas a model that assumed that katanin acts preferentially on spatially infrequent micr
33 urons with bFGF heightens expression of both katanin and spastin, which are proteins that sever micro
35 lating the microtubule response to stress in katanin and spiral2 mutant made sepal shape dependent on
39 protein that is recognized by an anti-human katanin antibody and that this protein is localized, at
43 tions in hereditary spastic paraplegias, and katanin are related microtubule-severing AAA ATPases inv
45 e identified the microtubule-severing enzyme katanin as a central player in controlling the organizat
53 nal growth is sensitive to the levels of P60-katanin, but that other factors contribute to modulating
55 tion mutations in the Caenorhabditis elegans katanin catalytic subunit, MEI-1, cause specific defects
58 MEI-1 may ensure temporal activation of the katanin complex during meiosis, whereas CRL3(MEL-26)-med
65 increasing microtubule density and a second, katanin-dependent phase that occurs after microtubule de
68 Consistent with this finding, GFP-tagged katanin driven by its native promoter localizes at sites
70 a mutation in the p80 regulatory subunit of katanin, encoded by the PF15 gene in Chlamydomonas, alte
72 mology domain protein encoded by aspm-1, the katanin family member mei-1, and the kinesin-12 family m
73 ase and Katanin p60-like 1 (Kat-60L1) of the Katanin family of microtubule severing proteins are requ
74 t of an E3 ubiquitin ligase complex, targets katanin for degradation during the transition from meios
75 Oligomerization increased the affinity of katanin for microtubules and stimulated its ATPase activ
78 tubule-severing proteins, p56, EF1alpha, and katanin, has only confused the issue because none of the
79 to encode a protein with high similarity to katanin (hence FRA2 was renamed AtKTN1), a protein shown
81 on with antibodies specific for a vertebrate katanin homologue to demonstrate that katanin is respons
82 roblasts to be more resistant to severing by katanin in a manner that was not dependent on the acetyl
83 and activity of the MT-severing protein p60-katanin in interneurons to promote the rapid remodeling
86 spindle shortening proceeds through an early katanin-independent phase marked by increasing microtubu
98 mmunofluorescence analysis demonstrated that katanin is concentrated at a microtubule-dependent struc
100 esults indicate that microtubule-severing by katanin is essential for releasing microtubules from the
101 rotubules at the centrosome, indicating that katanin is indeed required for microtubule release from
104 es on cultured sympathetic neurons show that katanin is present at the centrosome, but is also widely
105 that sensitivity to microtubule severing by katanin is regulated by a balance of factors, including
106 e sensitivity of microtubules to severing by katanin is regulated by acetylation of the microtubules.
110 ebrate katanin homologue to demonstrate that katanin is responsible for the majority of M-phase sever
113 Using various rat tissues, we found that P60-katanin levels are much higher than spastin levels durin
115 rodent brain, neurons vary significantly in katanin levels, depending on their developmental stage.
116 HDC5-deficient cells show an increase in p60/katanin levels, indicating that Cul3/Ctb9/KLHDC5 is requ
117 Taken together, these data suggest that a katanin-like mechanism may mediate the severing of the o
119 We further demonstrated that the Arabidopsis katanin-like protein possessed MT-severing activity in v
120 gether, these results suggest that AtKTN1, a katanin-like protein, is essential not only for normal c
123 found in adult mouse brain, indicating that katanin may have other functions distinct from its mitot
124 crotubules for a fixed pool of tubulin, with katanin-mediated severing allowing easier access to this
125 loped to enable the real-time observation of katanin-mediated severing of individual, mechanically un
126 ed that phototropin photoreceptors stimulate katanin-mediated severing specifically at microtubule in
127 er the microtubule-severing protein known as katanin mediates microtubule release from the neuronal c
131 eric protein phosphatase 4 complex, enhanced katanin MT-severing activity during C. elegans meiosis.
134 titative imaging experiments and analysis of katanin mutants showed that the longitudinal arrays are
135 r assay demonstrated that the p60 subunit of katanin oligomerized in an adenosine triphosphate (ATP)-
136 After hydrolysis of ATP, microtubule-bound katanin oligomers disassembled microtubules and then dis
139 required for transport) pathway and spastin, katanin p60 and fidgetin affecting multiple aspects of c
141 nown regarding the role of the family member Katanin p60 subunit A-like 1, KATNAL1, in central nervou
142 IS1 homology (LisH) motif, including several katanin p60 subunits, muskelin, tonneau, LEUNIG, Nopp140
144 irement for the microtubule-severing protein katanin p60-like 1 (Kat-60L1) in regulating the elaborat
145 Here, we show that both the Ik2 kinase and Katanin p60-like 1 (Kat-60L1) of the Katanin family of m
148 red that microtubule severing by the protein katanin plays a crucial and unexpected role in the reori
150 bules renders them notably less sensitive to katanin, prompting us to posit that microtubule disinteg
159 rt a model in which MBK-2 down-regulates the katanin-related protein MEI-1 to control spindle positio
161 croinjection of an antibody that inactivates katanin results in a dramatic accumulation of microtubul
163 f short microtubules, whereas the excess P60-katanin results in short microtubules intermingled with
164 ant MT orientation caused by the mutation of katanin results in the distorted deposition of cellulose
167 ults indicated that katanin protein, but not katanin's microtubule-severing activity, is required for
171 udy using electron tomography has found that katanin stimulates the production of microtubules in the
172 veral oocyte proteins, including the meiotic katanin subunit MEI-1 and the oocyte maturation protein
177 nstrate a novel regulatory mechanism for p60/katanin that occurs at the level of targeted proteolysis
179 e severing protein that shares homology with katanin, the microtubule severing activity of which prom
181 s of the microtubule-severing protein termed katanin to completely break down the axonal microtubule
182 the sufficient and necessary conditions for katanin to promote array alignment, stresses the critica
187 The microtubule-severing subunit p60 of katanin was identified as a candidate substrate for MAB1
189 To understand the nonsevering activities of katanin, we characterized the N-terminal domain of the k
190 nd functional similarity between spastin and katanin, we hypothesized that spastin promotes the dynam
191 tanin and regulated the severing activity of katanin, which cut the cellular microtubules into short
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