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1  by DcuABC in exchange for L-aspartate and L-malate.
2 s enhancing nocturnal CO2 fixation to stored malate.
3 ary RCH were treated with systemic sunitinib malate.
4 ylated sugar intermediates and of starch and malate.
5 rticularly the roles of starch, sucrose, and malate.
6 nce via a novel mechanism involving sinapoyl malate.
7 xpress the ME genes and is unable to utilize malate.
8 t, followed by the binding of oxaloacetate/L-malate.
9 building up the ester side chain to sinapoyl malate.
10 I) reduction in the presence of tartrate and malate.
11 ven glucose and pyruvate but normalized with malate.
12 cretion of organic acids such as citrate and malate.
13 apillary RCH treated with systemic sunitinib malate.
14 ncluding citrate, isocitrate, succinate, and malate (1.4-3.9-fold).
15       cbl1 plants exudated less Al-chelating malate, accumulated more Al, and displayed a severe root
16       These perturbations paralleled reduced malate accumulation at dawn and decreased nocturnal star
17                                              Malate accumulation in the vacuole largely determines ap
18 logical traits and drought-induced nighttime malate accumulation was observed across genotypes.
19 optimizing CAM-associated dark CO2 fixation, malate accumulation, CAM productivity, and core circadia
20 y, dark period CO(2) fixation, and nocturnal malate accumulation.
21 ctivated malate transporter 12 (ALMT12) is a malate-activated, voltage-dependent member of the alumin
22          The increased longevity provided by malate addition did not occur in fumarase (fum-1), glyox
23                                              Malate also increased NADPH, NAD, and the NAD/NADH ratio
24 VHL) disease treated with systemic sunitinib malate, an agent that inhibits both anti-vascular endoth
25         Ultraviolet spectroscopy of sinapoyl malate, an essential UV-B screening agent in plants, was
26 med) are 2.73 for oxidation of pyruvate plus malate and 1.64 for oxidation of succinate.
27  reduced Km [PEP] coupled with elevated I50 [malate and Asp] values) via in vivo deubiquitination of
28 ppc2 mutant greatly reduced the synthesis of malate and citrate and severely suppressed ammonium assi
29 h the PEP carboxylase competitive inhibitors malate and diethyl oxalacetate (DOA) in the strong isopr
30                                         Both malate and DOA did not alter the sensitivity of isoprene
31                                              Malate and fumarate addition increased oxygen consumptio
32 ls and nitrate, increased levels of sucrose, malate and fumarate and minor changes in total protein a
33 tribute to the lifespan extension induced by malate and fumarate by increasing the amount of oxidized
34  previously with an impaired accumulation of malate and fumarate in leaves.
35 lacking AtQUAC1 accumulated higher levels of malate and fumarate.
36 upplying the ppc1/ppc2 mutant with exogenous malate and glutamate, suggesting that low nitrogen statu
37  malate importer, ABCB14, increases both its malate and its background auxin transport activity, sugg
38 y DcuABC-mediated import and conversion of L-malate and L-aspartate.
39                                              Malate and lactate dehydrogenases (MDH and LDH) are homo
40                      Lactate levels, lactate/malate and lactate/pyruvate ratios were elevated in HKCs
41 pression of maeP and maeE is induced by both malate and low pH, and induction in response to both cue
42                    Some metabolites, such as malate and Man, appeared in the models for both conducta
43    Additional structures of the complex with malate and of the apo form of GlcB supported that hypoth
44 ially NADPH-producing pathways involving (S)-malate and ornithine, quorum sensing, sporulation, and c
45 n of RsbU revealed that alpha-ketoglutarate, malate and oxaloacetate bound to the RsbU periplasmic do
46 d is its catalysis of the interconversion of malate and oxaloacetate in the tricarboxylic acid cycle.
47 ine, aspartate, cysteine, glutamine, lysine, malate and pyroglutamate.
48                                              Malate and pyruvate were diverted to produce aspartate,
49   LND inhibits the formation of fumarate and malate and suppresses succinate-induced respiration of i
50 quently, this oxaloacetate is converted into malate and then pyruvate, ostensibly increasing the NADP
51 ng its sensitivity to feedback inhibition by malate and thus enhancing nocturnal CO2 fixation to stor
52 three different substrates (L(+)-tartrate, D-malate, and 3-isopropylmalate).
53 gulatory mechanism of BdALMT12 activation by malate, and Ca(2+)/CaM, emphasizing that a complex regul
54  of 19 traits, including sucrose, ascorbate, malate, and citrate levels.
55 tes including alpha-KG, succinate, fumarate, malate, and citrate were observed in TGF-beta1-different
56 ally relevant concentrations of pyruvate and malate, and flux of respiration, NAD(P)H fluorescence, a
57 ncomitant accumulation of the MDH substrate, malate, and fumarate, its immediate precursor in the Kre
58 itrate, 2-oxoglutarate, succinate, fumarate, malate, and oxaloacetate) were tested for their influenc
59 riptan, eletriptan hydrobromide, almotriptan malate, and rizatriptan benzoate tablets.
60 ull assimilatory flux to produce glyoxylate, malate, and succinate.
61 n rates in response to glutamate, but not to malate, and were depleted in all TCA cycle substrates be
62 s cell system confirmed that this channel is malate- and voltage-dependent.
63 ral function affording bacterial growth on D-malate as a carbon source, the D-malate dehydrogenase of
64 sIII, and is required for normal growth with malate as a sole carbon source.
65 umarate, so conversion of this metabolite to malate as detected by (13)C-magnetic resonance spectrosc
66  displayed lower production of aspartate and malate, as well as reduced k(pyr->asp) and (13)C-label e
67  (LDH) reaction and the intermediates of the malate-aspartate and glycerol 3-phosphate shuttles.
68 ism by which GOT2 acetylation stimulates the malate-aspartate NADH shuttle activity and oxidative pro
69 ere we find that the absence of a functional malate-aspartate NADH shuttle caused by aralar/AGC1 disr
70  mitochondria, is the regulatory step in the malate-aspartate NADH shuttle, MAS.
71 d increases the expression of glycolysis and malate-aspartate shuttle (MAS) genes.
72 r Aralar/AGC1 (Slc25a12), a component of the malate-aspartate shuttle (MAS), is stimulated by modest
73                 Here, we studied the role of malate-aspartate shuttle (MAS)-dependent substrate suppl
74 sport mechanisms with consequent compromised malate-aspartate shuttle and changes in allosteric effec
75 mplex I of the electron transport chain, the malate-aspartate shuttle and mitochondrial citrate expor
76  relies on shuttle mechanisms, including the malate-aspartate shuttle and the glycerol-3-phosphate sh
77 t a profound reliance on glucose metabolism, malate-aspartate shuttle deregulation leads to a specifi
78                                          The malate-aspartate shuttle is indispensable for the net tr
79                                          The malate-aspartate shuttle is operated by two pairs of enz
80 nd that mitochondrial citrate export and the malate-aspartate shuttle promote histone acetylation, an
81            Hyperacetylation of mitochondrial malate-aspartate shuttle proteins impaired the transport
82 drogenase (MDH) operate as components of the malate-aspartate shuttle, in which a reducing equivalent
83  These findings support a model in which the malate-aspartate shuttle, mitochondrial citrate export a
84                        GOT2, a member of the malate-aspartate shuttle, plays an essential role in the
85 partate/glutamate carriers is central to the malate-aspartate shuttle, urea cycle, gluconeogenesis an
86  Reduced levels of aspartate deregulated the malate-aspartate shuttle, which is important for cytopla
87 itochondrial transporter that is part of the malate-aspartate shuttle, which regulates the NAD+/NADH
88 ate carrier 1 (AGC1), a key component of the malate-aspartate shuttle.
89 ons, is the regulatory component of the NADH malate-aspartate shuttle.
90 eotide breakdown and partial reversal of the malate/aspartate shuttle.
91 he restoration of respiration with glutamate/malate back to control levels.
92  catalyze the oxidative decarboxylation of D-malate-based substrates with various specificities.
93                        The broader role of a malate/beta-methylmalate synthase in human physiology an
94               We report that CLYBL encodes a malate/beta-methylmalate synthase, converting glyoxylate
95 oascorbic (DHAA) acids and validated in 20mM malate buffer (pH 3.8).
96  studied: calcium carbonate, calcium citrate malate, calcium phosphate and calcium bisglycinate.
97                                              Malate can be synthesized from fumarate by the enzyme fu
98 haliana Our results also show that exogenous malate can rescue the long-root phenotype of lpi5 and lp
99 olonization assays to describe how aspartate/malate can trigger initial Salmonella Typhimurium gut-lu
100 lling the production of organic acid anions (malate, citrate) that are excreted in copious amounts by
101 hat chemically reduce iron(III) from citrate-malate complexes.
102 e roots constitutively and had 2-fold higher malate concentrations in the xylem sap than nulls, indic
103 3)C-label exchange rate between pyruvate and malate, consistent with down-regulated gluconeogenesis.
104        We demonstrate that fruit citrate and malate contents have been impacted by selection during d
105 esent bioinformatic data suggesting that the malate cycle may support phosphoglycolate salvage in div
106 that an oxidative pathway, which we term the malate cycle, supports phosphoglycolate salvage.
107                              The alternative malate decarboxylase, NADP-ME, did not appear to compens
108                     During the light period, malate decarboxylation concentrates CO(2) around Rubisco
109           Q2: Do the enzymes responsible for malate decarboxylation limit daytime mobilisation from t
110 ) catalyze two key steps during light-period malate decarboxylation that underpin secondary CO(2) fix
111                              The kinetics of malate dehydrogenase (MDH) catalyzed oxidation/reduction
112                            Two isoenzymes of malate dehydrogenase (MDH) operate as components of the
113 hosphate, reduced are used by NADP-dependent malate dehydrogenase (MDH) to reduce OAA to malate, thus
114                                              Malate dehydrogenase (MDH), a key enzyme in the tricarbo
115 tes aggregation of model substrates, such as malate dehydrogenase (MDH), and inhibits disaggregation
116 atured substrates such as alpha-lactalbumin, malate dehydrogenase (MDH), and the beta-subunit of ATP
117                   MDH2 encodes mitochondrial malate dehydrogenase (MDH), which is essential for the c
118  peroxisomal NADH is reoxidised to NAD(+) by malate dehydrogenase (Mdh3p) and reduction equivalents a
119                                Mitochondrial malate dehydrogenase (mMDH; EC 1.1.1.37) has multiple ro
120 as activated primary T cells, that cytosolic malate dehydrogenase 1 (MDH1) is an alternative to LDH a
121 X5 (PEX5C) receptor construct or peroxisomal malate dehydrogenase 1 (pMDH1) cargo protein into sunflo
122 d in cell-cell contacts) and MDH1 (cytosolic Malate dehydrogenase 1), revealed their role in early st
123 led to increased nitrogen assimilation, NADP-malate dehydrogenase activation, and light vulnerability
124                                           No malate dehydrogenase activity was detected using macerat
125 urs of NMP with URC, including mitochondrial malate dehydrogenase and glutamic-oxaloacetic transamina
126 n into two target proteins (Escherichia coli malate dehydrogenase and human histone H3) caused homoge
127  alanine amino transferase and glutamate and malate dehydrogenase and malate, there are no links betw
128 cytochrome-C) and others (creatine kinase M, malate dehydrogenase cytosolic, fibrinogen and parvalbum
129 HG is generated by lactate dehydrogenase and malate dehydrogenase in response to hypoxia.
130 growth on D-malate as a carbon source, the D-malate dehydrogenase of Escherichia coli (EcDmlA) natura
131                           The heat-denatured malate dehydrogenase that did not refold by the assistan
132 trate channeling (e.g., of oxaloacetate from malate dehydrogenase to citrate synthase), and use of al
133 rase and further oxidized to oxaloacetate by malate dehydrogenase with the accompanying reduction of
134 ctor protein (SteA), and a metabolic enzyme (malate dehydrogenase), and demonstrate practical applica
135 ycle components, including citrate synthase, malate dehydrogenase, and aconitase, resulted in a one-c
136 the metabolic enzymes citrate synthase (CS), malate dehydrogenase, and strombine dehydrogenase remain
137 d interfacial residues between mitochondrial malate dehydrogenase, citrate synthase, and aconitase we
138 es with isolated lactate dehydrogenase-1 and malate dehydrogenase-2 revealed that generation of 2-HG
139 d two key enzymes-glycerol dehydrogenase and malate dehydrogenase-were overexpressed to improve PA ti
140 hose substrates include the short-lived Mdh2 malate dehydrogenase.
141 nzymes with multiple isoforms, aconitase and malate dehydrogenase.
142 tamate oxaloacetate transaminases (GOT), and malate dehydrogenases (MDH).
143 nd MDH2 encoding mitochondrial and cytosolic malate dehydrogenases, respectively; and (iv) GLN1 encod
144                Lifespan extension induced by malate depended upon the longevity regulators DAF-16 and
145 )-ATO and Mito(10)-ATO inhibit both pyruvate/malate-dependent complex I and duroquinol-dependent comp
146  Nicotiana benthamiana cells, Ma1 mediates a malate-dependent inward-rectifying current, whereas the
147 e substrates between alpha-ketoglutarate and malate despite high rates of glutaminolysis, as determin
148 ion during therapy, treatment with sunitinib malate did not improve visual acuity or reduce the size
149           Despite these conditions, sinapoyl malate displays anomalous spectral broadening extending
150  that increasing OsALMT4 expression affected malate efflux and compartmentation within the tissues, w
151                                     Q3: Does malate efflux from the vacuole set the pace of decarboxy
152 ing the membrane permease ALMT1, to increase malate exudation in response to low phosphate.
153 cue the long-root phenotype of lpi5 and lpi6 Malate exudation is required for the accumulation of Fe
154 o underlie Arabidopsis Al tolerance via root malate exudation, known as SENSITIVE TO PROTON RHIZOTOXI
155         However, the rapid clearance of Sunb-malate eye drops administered through topical instillati
156 culates as ferric complexes with citrate and malate (Fe(III)3Cit2Mal2, Fe(III)3Cit3Mal1, Fe(III)Cit2)
157 ed included: iron complexes with citrate and malate: Fe(III)(Cit)(3)(Mal), Fe(III)(Cit)(2)(Mal)(2), F
158                                              Malate feeding resulted in the inhibition of net assimil
159        We detected signals from fumarate and malate following intravenous administration of hyperpola
160 e suture-induced corneal NV than either Sunb-malate free drug or the placebo MS.
161 anion channel responsible for the release of malate from guard cells, is essential for efficient stom
162    The active endobacterium likely extracted malate from the fungal host as the primary carbon substr
163 e lines overexpressing (OX) OsALMT4 released malate from the roots constitutively and had 2-fold high
164 of various metabolites including sucrose and malate (from several potential sources; including guard
165 schemia, PTP opening may result in succinate/malate-fueled ROS production from complex III due to act
166 ariation in several metabolite pools such as malate, fumarate or citrate, and flux calculations sugge
167 ne), tricarboxylic acid cycle intermediates (malate, fumarate), glutamate, fatty acid acylcarnitines,
168  sensitivity, including alpha-ketoglutarate, malate, fumarate, succinate, 2-hydroxyglutarate, citrate
169 ome metabolites, including Glc-6-P, Fru-6-P, malate, fumarate, Xyl, and ribose.
170 gen flux after the addition of glutamate and malate (GM), adenosine diphosphate (d), succinate (S) an
171 trate, isocitrate and the two enantiomers of malate have been studied by (1)H NMR titration experimen
172 ntrations of citrate, and to a lesser extent malate, have a major impact on nucleus-encoded transcrip
173 lts of this study collectively indicate that malate importantly controls the chloroplast reductive st
174        Introduction of this D/E-P motif into malate importer, ABCB14, increases both its malate and i
175 ive cardiac means to replenish succinate and malate in MS.
176  nulls, indicating greater concentrations of malate in the apoplast.
177 e CO(2) via an organic intermediate, such as malate in the case of C(4) CCMs).
178  the reversible oxidative decarboxylation of malate in the presence of NADP.
179 , KCS combinations of glutamate, citrate and malate increased PFP (from 1.22 to 1.29 mmol peroxides/k
180 ges in isoprene emission rate in control and malate-inhibited leaves were associated with changes in
181                                              Malate inhibition of isoprene emission was associated wi
182  convert the C4-dicarboxylates aspartate and malate into fumarate (AspA, FumABC), are required for fu
183 nt analyses of doubly tagged, doubly charged malate ions.
184                                              Malate is a central metabolite involved in a multiplicit
185                               Cabozantinib S-malate is a vascular endothelial growth factor receptor
186 sides the active site, where the substrate S-malate is bound bidentate to the unique iron of the [4Fe
187                         The role of sinapoyl malate is confirmed through the use of a mutant compromi
188  or carbonyl carboxylates, such as tartrate, malate, lactate, pyruvate, and mandelate, significantly
189             The oxaloacetate is converted to malate, leading to malic acid accumulation in the vacuol
190 e calli results in a significant decrease in malate level.
191 h was coordinated predominantly by phosphate/malate ligands.
192                            We developed Sunb-malate loaded poly(D,L-lactic-co-glycolic acid) (PLGA) m
193 at night for the mesophyll to fix CO(2) into malate (Mal) and store it in the vacuole.
194                           Systemic sunitinib malate may be useful in slowing progression of ocular di
195 in this small series, and systemic sunitinib malate may not be safe for treatment of RCH when used at
196 ains predicted to impact the activity of the malate metabolic pathway.
197  Kok break point is also probably related to malate metabolism, which participates in maintaining pho
198 lly rate-limiting steps underpinning diurnal malate mobilisation and help direct future research effo
199 ion of CO(2) via RuBisCo dictate the rate of malate mobilisation?
200 ght-time primary carboxylation reactions and malate movement across the tonoplast.
201                                         Sunb-malate MS following SCT injection more effectively suppr
202 unb-malate through the SCT injection of Sunb-malate MS mitigated the proliferation of vascular endoth
203      Subconjunctival (SCT) injection of Sunb-malate MS provided a prolonged ocular drug retention and
204                                         Sunb-malate MS sustained the drug release for 30 days under t
205 -co-glycolic acid) (PLGA) microspheres (Sunb-malate MS) with a particle size of approximately 15 mum
206 greatly neutralized by SCT injection of Sunb-malate MS.
207 ose, lactate, alanine, glycerol 3-phosphate, malate, myo-inositol, or stearic acid tissue concentrati
208 l b, fructose, fumarate, glucose, glutamate, malate, nitrate, starch, sucrose, total amino acids, and
209 he dark or in nonphotosynthetic tissues, the malate-OAA shuttle was proposed to be mediated by the co
210 ivery pathways to the bundle sheath (BS; via malate or aspartate), and rates of phosphoglyceric acid
211  the predominance of Mn(II), bound mostly to malate or citrate, in roots and stems of all four specie
212 mulated in vacuoles as either soluble Mn(II) malate or citrate.
213 ochondria (n = 7) for glycolysis (pyruvate + malate)- or FA (palmitoylcarnitine)-derived substrates,
214 bution of isotopes when (13)C-glucose, (13)C-malate, or (13)C-pyruvate was provided as a substrate to
215 ure following incubation with abscisic acid, malate, or citrate.
216 ase, converting glyoxylate and acetyl-CoA to malate, or glyoxylate and propionyl-CoA to beta-methylma
217  in lipid vesicles catalyzed the exchange of malate, oxaloacetate, and aspartate for phosphate plus a
218 graphic analyses with succinate, fumarate, L-malate, oxaloacetate, pyruvate and D- and L-2HG support
219 duction-oxidation (redox) homeostasis is the malate-oxaloacetate (OAA) shuttle.
220 ase (MDH) catalyzed oxidation/reduction of L-malate/oxaloacetate is pH-dependent due to the proton ge
221  found that in glucose grown cells, both the malate/oxaloacetate shuttle and a glycerol-3-phosphate d
222 alents are transferred to the cytosol by the malate/oxaloacetate shuttle.
223  required for expression of genes encoding a malate permease (maeP) and malic enzyme (maeE).
224                                            A malate-phosphate anti-porter DctA is regulated by RpoN a
225  hydrogen peroxide emission using pyruvate + malate (PM) or succinate + rotenone (SR) as substrates.
226 ing in increased [(13)C]-glucose flux toward malate production, potentially explaining the susceptibi
227 ing to cytosolic glucose carbon flow via OAA-malate-pyruvate and acetyl-CoA-fatty acid pathways in TR
228            First, expression of the putative malate-pyruvate NADH shuttle increases in ssy5Delta cell
229      Here, we investigate the staphylococcal malate-quinone and l-lactate-quinone oxidoreductases (Mq
230                 We solved the structure of a malate racemase apoprotein and used it, along with the p
231                            We discovered two malate racemases, one phenyllactate racemase, one alpha-
232 s known regarding the drivers behind diurnal malate remobilisation from the vacuole that liberates CO
233                           In the presence of malate, RoxS transiently escapes from repression by the
234 ALMT and AtMATE, responsible for citrate and malate secretion, respectively, were elevated under Ga s
235 atives most closely associated with sinapoyl malate showing characteristic broadening even under jet-
236 ngstrom crystal structure of MatC with bound malate shows a high level of substrate coordination, wit
237                    Particularly, the citrate-malate shuttle supplies cytosolic acetyl-CoA and plastid
238 ralar deficiency, presumably through citrate-malate shuttle.
239 racteristics brought on by the electron-rich malate side chain.
240  altered as reflected by increased nighttime malate, starch, and glutathione levels and a reduced res
241 induced changes in amino acids, fumarate and malate, suggesting Krebs cycle up-regulation.
242                                    Sunitinib malate (Sunb-malate) targeting against multiple receptor
243                                              Malate supplementation did not extend the lifespan of lo
244    We have used a fragment-based approach on malate synthase (GlcB) from Mycobacterium tuberculosis a
245                         Here, we report that malate synthase (MS), the second enzyme of the glyoxylat
246 lidated the increase in isocitrate lyase and malate synthase activities.
247  as an essential physiologic function of Mtb malate synthase and advances its validation as a target
248 tudy the genes encoding isocitrate lyase and malate synthase from Chlorogloeopsis fritschii PCC 9212
249 g pathway of an 82-kDa slow folding protein, malate synthase G (MSG), was investigated.
250 anscript abundances for isocitrate lyase and malate synthase increased, and C. fritschii grew faster,
251 When the genes encoding isocitrate lyase and malate synthase were expressed in Synechococcus sp. PCC
252 glyoxylate shunt genes (isocitrate lyase and malate synthase) was >300-fold higher in the light--but
253 orted the activities of isocitrate lyase and malate synthase, the key enzymes of the glyoxylate cycle
254                                              Malate synthases are best known for their established ro
255                       Sunitinib malate (Sunb-malate) targeting against multiple receptor tyrosine kin
256 showed a stronger interaction with dianionic malate than with the trianionic citrate or isocitrate, s
257 conversion of hyperpolarized oxaloacetate to malate, the two signal components are separated into com
258                                         Sunb-malate, the water-soluble form of sunitinib, was shown t
259 e and glutamate and malate dehydrogenase and malate, there are no links between single enzyme activit
260  in hydroponics but, when combined with 1 mm malate, this concentration inhibited growth.
261              Local sustained release of Sunb-malate through the SCT injection of Sunb-malate MS mitig
262  malate dehydrogenase (MDH) to reduce OAA to malate, thus regenerating the electron acceptor NADP.
263 rgillus carbonarius, AcDct(p), increased the malate titer 12-fold without affecting the growth.
264  the malic enzyme (ME) pathway, which allows malate to be used as a supplemental carbon source for gr
265 H), which is essential for the conversion of malate to oxaloacetate as part of the proper functioning
266 carboxylases that catalyse the conversion of malate to pyruvate and are essential for NADPH regenerat
267  fumarate with a progressive increase in the malate-to-fumarate (MA/FA) ratio at days 2 to 5 after so
268  indicating that ma1 has significantly lower malate transport activity than Ma1.
269         This study reveals new links between malate transport and mineral nutrition.
270 hat the truncation of Ma1 to ma1 reduces its malate transport function by removing a conserved C-term
271                                     Vacuolar malate transport has been characterized at the molecular
272 ON RHIZOTOXICITY1 (STOP1)-ALUMINUM-ACTIVATED MALATE TRANSPORT1 (ALMT1) signaling module was tested th
273 anion flux through plant aluminium-activated malate transporter (ALMT) proteins is activated by anion
274 RHIZOTOXICITY (STOP1) and ALUMINUM ACTIVATED MALATE TRANSPORTER 1 (ALMT1), represent a critical check
275                       The aluminum-activated malate transporter 12 (ALMT12) is a malate-activated, vo
276 e-dependent member of the aluminum-activated malate transporter family that has been implicated in an
277 nts degradation of the yflS mRNA, encoding a malate transporter.
278 m genes, including carbonic anhydrases and a malate transporter.
279 unction analysis is shown using the aluminum malate transporter1 gene.
280  identification of ALMT4 (ALUMINUM ACTIVATED MALATE TRANSPORTER4) as an Arabidopsis thaliana ion chan
281 on of Ma1, an ortholog of ALUMINUM-ACTIVATED MALATE TRANSPORTER9 (ALMT9) in Arabidopsis (Arabidopsis
282                           Aluminum-activated malate transporters (ALMTs) form a family of anion chann
283                       The aluminum-activated malate transporters (ALMTs) form a membrane protein fami
284 of plastid-cytosol and mitochondrion-cytosol malate transporters in recycling the ammonia liberated d
285 sophyll of isozymes implicated in starch and malate turnover are discussed in line with the contrasti
286                                 Furthermore, malate uptake and utilization contribute to the adaptive
287 o S. pyogenes' carbon source repertory, that malate utilization is a highly regulated process, and th
288                                Additionally, malate utilization requires the PTS transporter EI enzym
289 s suggest that other mechanisms, such as the malate valve and the Mehler reaction, were able to maint
290                       Hence, the chloroplast malate valve and triose phosphate-3-phosphoglycerate shu
291 glucose, fructose, sucrose, starch, citrate, malate, vitamin C and soluble and insoluble oxalic acid.
292 e, induced by exogenous Ca(2+) ionophore and malate, was shown to be inhibited by exogenous applicati
293 ntration, in the presence of L-carnitine and malate, were performed.
294 n 2-day hypoxia and is mediated by cytosolic malate whereas in 10-day hypoxia the rewiring is mediate
295 o the active mechanism intrinsic to sinapoyl malate, which is tentatively attributed to mixing of the
296  with acetyl coenzyme A (acetyl-CoA) to give malate, which undergoes two oxidative decarboxylation st
297 ich a reducing equivalent is transported via malate, which when oxidized to oxaloacetate, transfers a
298 er, our results indicate that MDH1 generates malate with carbons derived from glutamine, thus enablin
299  protein from this system, binds to l- and d-malate with K(d) values of 27 and 21 nM, respectively, t
300 p. palustris, grew photoheterotrophically on malate without electron acceptors or H2 production.

 
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