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1 t accommodates one calcium ion in its fourth EF-hand.
2 sion of a single precursor lobe of a pair of EF-hand.
3 lin-like domain (CamLD) with calcium-binding EF hands.
4 th calcium-dependent and calcium-independent EF hands.
5 cs by disrupting beta-sheet coupling between EF hands.
6 tion where the PH domain moves away from the EF hands.
7 mboid protease that harbours calcium-binding EF-hands.
8 EF-2, EF-1 and allostery involving the four EF-hands.
9 are pollen-specific proteins containing two EF-hands.
10 th calcium-dependent and calcium-independent EF-hands.
11 influence the structure of the metal-binding EF-hands.
12 hands 1 and 4 as well as the linkers before EF hand 1 and the linkers between EF hands 4 and 5 and E
13 ation in combination with mass spectrometry, EF hands 1 and 4 as well as the linkers before EF hand 1
14 h formed by the surface of non-metal-binding EF-hand 1, the loop and the exiting helix of EF-hand 2,
15 nity for calcium ions of visinin-like domain EF-hands 1 and 2 (K(d) = 200 +/- 50 nM) was appropriate
18 Under the experimental conditions employed, EF hands 2 and 6, which are known not to bind calcium, w
20 the flexibility of the hinge region between EF-hands 2 and 3 is required for placing GCAP1-regulated
21 FA titration experiments revealed that NCS-1 EF-hands 2-4 (EF2-4) contributed to binding with the D2R
22 um oscillations (~125-850 nM), while that of EF-hand 3 (K(d) </= 20 nM) implied occupancy at basal ca
24 ha-helix, and the C-terminal lobe containing EF-hands 3 and 4 of VILIP-2 are sufficient to transfer i
25 ers before EF hand 1 and the linkers between EF hands 4 and 5 and EF hands 5 and 6 were identified as
26 ly reduced the affinity of Ca(2+) binding to EF-hand 4 and Ca(2+) sensitivity of the cyclase regulati
27 n the C-terminal portion of GCAP1, including EF-hand 4 and the helix connecting it with the N-termina
28 (or "tug") between the fatty acyl group and EF-hand 4 via the C-terminal helix that attenuates the e
32 and the linkers between EF hands 4 and 5 and EF hands 5 and 6 were identified as regions of conformat
33 EF hand 2 is highly accessible; however, EF hand 6 was determined not to be surface accessible in
34 atory domain containing four calcium-binding EF-hands, a linker loop domain with an amphipathic alpha
35 lcium-regulated N-terminal domain with eight EF-hands, a mitochondrial carrier domain, and a C-termin
36 Interestingly, deleting the amino-terminal EF-hands activates proteolysis prematurely, while residu
37 hemotaxis was unaffected when Ca(2)+-binding EF hands and a conserved phosphorylation site of RGEF-1b
41 lasmic Na(V) C-terminal region including two EF-hands and an IQ motif, the Na(V) domain III-IV linker
42 Surprisingly, we find that the C-terminal EF-hands and coiled-coil domains do not contribute to PK
43 opathy or cancer that targeted the canonical EF hand, and the hydrophobic cleft yielded constitutivel
44 have a coiled-coil adaptor domain, a pair of EF-hands, and a Rab GTPase fused into a single polypepti
45 t PC2 channels unable to bind Ca(2+) via the EF-hand are inactive in single-channel planar lipid bila
50 in the radius of gyration (R(g)) of the PC2 EF-hand by small angle x-ray scattering and significant
51 tions, ChREBP interacts with sorcin, a penta EF hand Ca(2+) binding protein, and is sequestered in th
52 model and analogous to crystal structures of EF hand Ca(2+)-binding proteins, two carboxylates (Asp-2
55 diac gene delivery of parvalbumin (Parv), an EF-hand Ca(2+) buffer, has been studied as a therapeutic
58 is a widely expressed, 22-kDa myristoylated EF-hand Ca(2+)-binding protein that shares a high degree
61 mologous proteins (CHP) are N-myristoylated, EF-hand Ca(2+)-binding proteins that regulate multiple c
65 titution (ParvE101Q) at amino acid 12 of the EF-hand Ca(2+)/Mg(2+) binding loop disrupts bidentate Ca
67 of the parvalbumin family, relative to other EF-hand CaBPs in cochlear and vestibular organs in the m
68 -induced calcium flash activates DUOX via an EF hand calcium-binding motif and thus triggers the prod
70 Gene-level enrichment analysis identified EF-hand calcium binding domain 14 as a novel susceptibil
75 nlike other reports of genetic disruption of EF-hand calcium buffers, deletion of oncomodulin (Ocm),
79 rvalbumin, calbindin, calretinin, N-terminal EF-hand calcium-binding protein 1, cholecystokinin, reel
80 Here we demonstrate that antibodies for the EF-hand calcium-binding protein, secretagogin, strongly
81 ion when compared with the apo states of the EF-hand calcium-binding proteins calmodulin, S100B, and
83 h about 20 members in humans, is composed of EF-hand calcium-regulated proteins and is linked to a ra
84 and functional studies showed that the first EF hand can only bind calcium and be functionally active
86 Ca(2+) and Mg(2+) binding to the individual EF-hands, characterize metal-induced conformational chan
88 motility-signaling connections, since EFHC1 (EF-hand containing 1), a potential PACRG interaction par
91 oupling proteins 2 and 3, the leucine zipper-EF-hand containing transmembrane protein 1 and the mitoc
92 ne protein 1-independent to a leucine zipper-EF-hand containing transmembrane protein 1- and mitochon
93 cium uniporter-dependent, but leucine zipper-EF-hand containing transmembrane protein 1-independent t
95 LC25A24, and SLC25A25--represent a family of EF-hand-containing mitochondrial proteins that transport
97 to identify MICU1 (also known as CBARA1), an EF-hand-containing protein that serves as a putative reg
99 l Na/Ca exchanger) and LETM1 (leucine zipper-EF-hand-containing transmembrane protein 1) were propose
101 Calmodulin-like (CML) proteins are major EF-hand-containing, calcium (Ca(2+))-binding proteins wi
104 tetrameric oligomeric state in which a fused EF hand domain arranges around the catalytic PPase domai
106 otion in PLC-beta by cross-linking it to the EF hand domain inhibits stimulation by Gbetagamma withou
108 B1-interacting partners identified a related EF hand domain-containing protein, calcineurin B, the re
109 ail consists of three functional regions: an EF-hand domain (PC2-EF, 720-797), a flexible linker (798
110 postulate the relative reorientation of the EF-hand domain and the IQ domain as a possible conformat
111 ns in the cationic residues within the first EF-hand domain and the XY linker region dramatically red
112 the EF-hand motifs or deletion of the entire EF-hand domain did not affect the Ca(2+)-dependent activ
114 We show that the binding of FHFs forces the EF-hand domain in a conformation that does not allow bin
115 servations highlight the central role of the EF-hand domain in modulating the binding mode of CaM.
119 These results indicate that, although the EF-hand domain is not required for RyR2 activation by cy
122 aracterized binding interactions between the EF-hand domain of alpha-actinin (Act-EF34) and peptides
125 of the net positive charge within the first EF-hand domain of PLCzeta significantly alters in vivo C
126 r SOICR termination, whereas deletion of the EF-hand domain of RyR2 increased both the activation and
127 ntly, single amino acid substitutions in the EF-hand domain of SEPN1 identified as clinical variation
128 h an amino acid substitution in a functional EF-hand domain or a truncation of this motif by aberrant
133 a(2+) binding to its canonical binding site (EF-hand domain) of polycystin 2, a Ca(2+)-dependent chan
134 in the PC2 Cterm, there is a calcium-binding EF-hand domain, crucial for the calcium-dependent activi
135 2 has been shown to contain a Ca(2+)-binding EF-hand domain, the molecular basis of PC2 channel gatin
136 ure has the overall architecture of a paired EF-hand domain, the NaV1.2 C-terminal domain does not bi
147 SAXS data suggest structural flexibility in EF hand domains indicative of conformational plasticity
151 substitution in a "hinge" region connecting EF-hand domains 2 and 3 in GCAP1 strongly interfered wit
152 S, and p.L151F), which are located on/around EF-hand domains 3 and 4, were confirmed as "pathogenic",
156 fferential calcium binding affinities of the EF-hand domains compared with those of CaM suggest that
159 Furthermore, we show that the Ca(2+)-sensing EF-hand domains of Miro1 are important for regulating mi
160 ty to bind free calcium, via calcium binding EF-hand domains on the protein, or to bind calcium compl
162 ized to different structural elements of the EF-hand domains suggest that Ca(2+)-induced folding is i
163 sidues within the canonical and noncanonical EF-hand domains that can bind to multiple Ca(2+) ions.
166 we show that two of the four calcium binding EF-hands dominate the FRET output of TN-XXL and that loc
168 function of the ABD and that the C-terminal EF hands (EF(34)) may bind to the linker that connects t
169 leckstrin homology (PH) domain and first two EF hands (EF1/2) are required for Rap1A activation and i
170 each containing one canonical Ca(2+)-binding EF-hand (EF1, EF4) and one structural EF-hand (EF2, EF3)
173 t structural differences occur in the fourth EF-hand (EF4) and adjacent helical region (residues 164-
174 ecretagogin, a recently cloned member of the EF-hand family of calcium binding proteins, was localize
175 trins (CETN1-4) are ubiquitous and conserved EF-hand-family Ca(2+)-binding proteins associated with t
176 H/DX results the deuterium patterns for each EF hand for each state of the protein (apo through fully
178 bstitution that had been presumed to destroy EF-hand function, that of glutamine for glutamate at pos
181 ubfamilies use different folds (coiled-coil, EF-hand, HOOK domain) and different surface contacts to
182 the four active sites for metal-ion binding (EF hands I, II, III, and IV) and the linker region (pept
184 conserved Phe residues at the -4 position in EF-hand III (F[-4]; Tyr(81)) and at the 13th position in
186 variant, Rasgrp1(Anaef), with an ENU-mutated EF hand in the Rasgrp1 Ras guanine nucleotide exchange f
187 From these results, we suggest that the EF hands in the C-lobe are flexible and can be thought o
188 xt showed that coordination of calcium by an EF-hand in ELC1 and prebinding of MLC1 to the MyoA neck
190 different relative binding affinities of the EF-hands in the engineered fragment compared with the in
194 (F[-4]; Tyr(81)) and at the 13th position in EF-hand IV (F[+13]; Phe(129)) of the C-terminal domain.
196 tion destabilises the native conformation of EF-hand IV, leading to a transient unfolding and dissoci
200 CaM)-binding IQ motif and the Ca(2+) sensing EF hand-like (EFL) motif in the carboxyl terminus of the
201 ormatics screening, we identified a putative EF-hand-like Ca(2+) binding motif in the carboxyl termin
202 modified beta-propeller fold and a distinct EF-hand-like calcium-binding site conserved in pathogens
204 cated within the second RCK domain, forms an EF-hand-like motif and is strategically positioned close
205 discovered a characteristic calcium-binding EF-hand-like motif in NS2 and found that the calcium bin
206 icated that Ca(2+) binding to the N-terminal EF-hand-like motif promotes the activity of SPCA1a by fa
207 th1.14-3-3 complex and the importance of the EF-hand-like motif were investigated using site-directed
208 a at least partially depend on an N-terminal EF-hand-like motif, which is present only in the SPCA1a
209 talytic domain and the region containing the EF-hand-like motif, whose role in the activation of Nth1
212 itions of bound Mg(2+) and Mn(2+) within the EF-hand loops are similar to those of Ca(2+); however, t
213 inase-inducible domain peptides are based on EF-hand loops in which a structurally critical Glu12 res
214 ain does not bind Ca2+ through the canonical EF-hand loops, as evidenced by monitoring 1H,15N chemica
216 among its four Ca(2+)-binding sites, called EF-hands, may contribute to CaM's functional versatility
217 exhibits low homology (30-40%) to the pseudo-EF-hand mitochondrial SCaMCs buffering/solute transport
226 alpha-helix (H6) and the proximal structured EF-hand motif using transition-metal ion fluorescence re
232 Ca(2+) binding domain encompassing a pair of EF-hand motifs (EF1 and EF2) in the skeletal muscle ryan
233 ) superfamily that harbors two high affinity EF-hand motifs and a C-terminal transmembrane domain.
234 y of Ca(2+) signaling in health and disease, EF-hand motifs designed to have new biological activitie
241 of Medicago truncatula CCaMK, which contains EF-hand motifs, or this domain together with the autoinh
242 toyl group on a long N-terminal arm and four EF-hand motifs, three of which bind Ca2+, assembled into
245 ent compared with the intact odd-even paired EF-hands (nCaM and cCaM) in terms of changes in flexibil
246 Ca(2+) and Mg(2+) binding to the individual EF-hands, observed metal-induced conformational changes,
249 studies revealed that Ca(2+) binding to the EF-hands of hSCGN induces significant structural changes
250 we found that in the presence of Ca(2+) the EF-hands of human plastins bound to an immediately adjac
251 tial pathway that favors the calcium binding EF-hands of the C-terminal lobe over those of the N-term
252 g in the high-affinity Ca(2+)-binding sites (EF-hands) of the GUCA1A gene encoding guanylate cyclase-
254 ane helices interacts intimately with paired EF-hands originating from the alpha-solenoid scaffold, s
255 elate with increased molecular motion in the EF-hand, possibly due to exchange between apo and Ca(2+)
256 as a point mutation in the calcineurin-like EF hand protein 1 (Chp1) gene that resulted in the produ
258 cover the IMAC, we have identified the small EF-hand protein calmodulin-like protein 4 (CALML4) as an
259 n neuronal calcium sensor-1, a multispecific EF-hand protein involved in neurotransmitter release and
260 Here, we studied the function of At-MICU, an EF-hand protein of Arabidopsis thaliana with homology to
261 that F1 TnC is a typical collapsed dumbbell EF-hand protein that accommodates one calcium ion in its
262 1) is an intrinsically disordered "imitator" EF-hand protein that increases the number of calcium car
263 This work focused on S100A11, a dimeric EF-hand protein with two hydrophobic target binding site
266 teraction of DREAM/KChIP3 with the important EF-hand protein, CaM, and show that the interaction alte
267 t conformational change into a high-affinity EF-hand protein, furnishing a mechanism by which the pro
269 onistic modulator (DREAM/KChIP3), a neuronal EF-hand protein, modulates pain, potassium channel activ
272 nctions of the members of the S100 family of EF-hand proteins are modulated by calcium and, in a numb
275 S100B is a member of the S100 subfamily of EF-hand proteins that has been implicated in malignant m
276 conductive channel while MICU1 and MICU2 are EF-hand proteins that regulate the channel activity in a
279 with a deletion of the entire N-terminal non-EF hand region still retains the LMAN1-binding function.
281 rgets CDPK2 to amylopectin stores, while the EF-hands regulate CDPK2 kinase activity in response to C
284 on of the Ca(2+)-binding residues within the EF hands resulted in a complete loss of PLS3 rescue.
285 and location of calcium-binding sites in the EF hand senses the concentration of calcium required for
286 This protein possesses a modified pseudo-EF-hand sequence at the C-terminal end which exhibits lo
291 calcium binding proteins that belong to the EF-hand superfamily with diverse biological functions.
293 ondrial inner membrane and has two canonical EF hands that are essential for its activity, indicating
294 determined the order of binding to the four EF hands to be III, IV, II, and I by extracting from the
295 Ca(2+) store depletion destabilized the two EF hands, triggering disassembly of the hydrophobic clef
296 abundant allergenic protein domain families (EF-hand, Tropomyosin, CAP, Profilin, Lipocalin, Trypsin-
297 dumbbell-shaped molecule that contains four EF hands (two in the N-lobe and two in the C-lobe) that
298 escence anisotropy (FA) and a panel of NCS-1 EF-hand variants to interrogate the interaction between
300 ding its myristoylation site, and the second EF-hand, which is inactive in Ca(2+) binding, are the ke