ライフサイエンスコーパス: light chain

1 28/PLIN-1 was found to bind to DLC-1 (dynein light chain).

2 upper hinge region, the CH1 domain, and the light chain.

3 ntire EMB motor domain bound to an essential light chain.

4 ine genes and be located in the heavy or the light chain.

5 of hydrogen peroxide by the VL domain of the light chain.

6 ice with a mutation in the myosin regulatory light chain.

7 of the disulphide bridge connecting with the light chain.

8 rates via reduction of phosphorylated myosin light chain.

9 ent for a pre-BCR and pairing with surrogate light chain.

10 derived heavy chain and a C terminus-derived light chain.

11 pairing of each heavy chain with its cognate light chain.

12 d fibrils derived from a particular antibody light chain.

13 nd lower expression of phosphorylated myosin light chain.

14 between Myo1 and its associating calmodulin light chains.

15 eterodimer and a block of two RB and six LC8 light chains.

16 ane-bound heavy chains (mHC) and 2 identical light chains.

17 l factors driving the amyloidogenesis of the light chains.

18 e VH of the VRC01 antibody but diverse mouse light chains.

19 th proteinuria composed mainly of free kappa light chains.

20 rophobic clusters distributed across CDRs of light chains.

21 o1C and the regulatory potential of atypical light chains.

22 s disrupt an interaction of INF2 with dynein light chain 1, a key dynein component.

23 gE-reactive protein was identified as myosin light chain 1, designated Gallus domesticus 7 (Gal d 7).

24 ity is enhanced by phosphorylation of myosin light chain 2 (MLC2) by cardiac-specific MLC kinase (cML

25 nd permeability via the Rho-dependent myosin light chain 2 and vascular endothelial (VE)-cadherin axi

26 The fast skeletal myosin regulatory light chain 2 followed by other five interacting protein

27 ecreased in MetSyn lymphatic vessels, myosin light chain 20, MLC(20) phosphorylation was increased in

28 proteins myosin heavy chain alpha and myosin light chain 2a in real-time during early differentiation

29 1, and microtubule-associated proteins 1A/1B light chain 3 (LC3) at baseline and post-AKI, which were

30 is induced significantly increased levels of light chain 3 (LC3) form II (LC3-II) and LC3 puncta in A

31 protein microtubule-associated protein 1A/1B light chain 3 (LC3)(1) and the disease-causing protein m

32 ession of the microtubule-associated protein light chain 3 (LC3), the autophagosomal membrane-associa

33 syn and led to an accumulation of endogenous light chain 3 (LC3)-positive puncta.

34 dulation of microtubule-associated protein 1 light chain 3 (LC3).

35 asuring microtubule-associated protein 1A/1B-light chain 3 (LC3)BII/I expression and autophagosome fo

36 Microtubule-associated protein 1 light chain 3 alpha (LC3)/GABA type A receptor-associate

37 s increased microtubule-associated protein 1 light chain 3 beta-II (LC3B-II) lipidation and induced s

38 he MAP1LC3 (microtubule-associated protein-1 light chain 3) family and the GABA receptor-associated p

39 including microtubule-associated protein 1B-light chain 3, autophagy-related protein (ATG)7, ATG2b,

40 ation reduced microtubule-associated protein light chain 3-mediated mitochondria clearance (mitophagy

41 (ATG9), a lipid scavenging protein, and LC3 (light-chain 3), which is involved in membrane curvature.

42 he autophagic protein microtubule-associated light chain-3 (LC3).

43 marker microtubule-associated proteins 1A-1B light chain 3B was increased in the double ROCK knockout

44 3B-II [microtubule-associated proteins 1A/1B light chain 3B-II] formation) followed by extrinsic apop

45 LC3B (LC3B; microtubule-associated protein 1 light chain 3beta) to peroxisomes in wild-type, but not

46 al phenotypes in both models of MYL4 (myosin light chain 4)-related atrial cardiomyopathy.

47 e in all patients, with a predominant lambda light chain (73%).

48 Dynein light chain 8 (LC8) interacts with intrinsically disorde

49 In this disease, monoclonal heavy and light chains accumulate in the lysosome of macrophages,

50 The mechanisms by which light-chain aggregation occurs are not well understood.

51 Overall, 25% of patients with immunoglobulin light chain (AL) amyloidosis die within 6 months of diag

52 In amyloid light chain (AL) amyloidosis, a small B-cell clone, most

53 Although no therapies are approved for light chain (AL) amyloidosis, cyclophosphamide, bortezom

54 Systemic antibody light chains (AL) amyloidosis is characterized by deposi

55 Immunoglobulin light-chain (AL) amyloidosis affects multiple systemic o

56 t of myeloma, but its efficacy and safety in light-chain (AL) amyloidosis has not been formally studi

57 To report an unusual case of light-chain (AL) amyloidosis with progressive bilateral

58 (MDex) were considered a standard of care in light-chain (AL) amyloidosis.

59 promising first results in systemic amyloid light-chain (AL) amyloidosis.

60 ments exist for relapsed/refractory systemic light-chain (AL) amyloidosis.

61 e natively paired, variable region heavy and light chain amplicons and the transcriptome of B lymphoc

62 tructural Determinants of the Immunoglobulin Light Chain Amyloid Aggregation", published in Physical

63 cal context and the crucial need to rule out light chain amyloid cardiomyopathy.

64 ive at clearing the material; however, human light chain amyloid extract, injected subcutaneously int

65 rate the heart are monoclonal immunoglobulin light-chain amyloid and transthyretin amyloid.

66 amples from 13 patients with pulmonary kappa light chain amyloidosis ((p)AL amyloidosis) used as cont

67 Immunoglobulin light chain amyloidosis (AL amyloidosis) is caused by mi

68 tive disorder, which could be complicated by light chain amyloidosis (AL) amyloidosis.

69 In light chain amyloidosis (AL), fibrillar deposition of mo

70 In systemic light chain amyloidosis, an overexpressed antibody light

71 tients, 64 (40%) had an MGRS lesion; amyloid light chain amyloidosis, the most common finding, accoun

72 ransthyretin, but an idiosyncratic effect in light chain amyloidosis.

73 tracellular volume in transthyretin, but not light chain amyloidosis.

74 tracellular volume in transthyretin, but not light chain amyloidosis.

75 Bortezomib is a standard therapy in light-chain amyloidosis (AL), but little is known about

76 nt and hypotension dominate the prognosis of light-chain amyloidosis (AL).

77 ssed by plasma cells in multiple myeloma and light-chain amyloidosis (AL).

78 Transthyretin and light-chain amyloidosis are the 2 main causes of cardiac

79 rs, the available treatments, especially for light-chain amyloidosis but also for several of the unde

80 Immunoglobulin light-chain amyloidosis is a protein aggregation disease

81 of a patient suffering from systemic amyloid light-chain amyloidosis, revealed a high degree of homog

82 proxies of neuronal integrity (Neurofilament light chain and phosphorylated heavy chain), DNA oxidati

83 n permeability via phosphorylation of myosin light chain and subsequent shrinkage of human brain endo

84 8 kDa), with a sequence coverage of 100% for light chains and 85% for heavy chains, demonstrating the

85 dation machinery, as well as secretion of Ig light chains and of cytokines and chemokines known to pr

86 tibodies and also smaller antibodies lacking light-chain and CH1 domains.

87 including ik2/TBK1, cut up (encoding dynein light chain) and hook, as genetic modifiers of FTD3-asso

88 acting proteins including Spn-F, Ik2, dynein light chain, and Hook, an adaptor protein in early endos

89 Q myosin mutation, phosphorylation of myosin light chains, and an increased ADP:ATP ratio, destabiliz

90 y, whose members generate conventional heavy/light-chain antibodies and also smaller antibodies lacki

91 We characterized the heavy chain and kappa light chain antibody repertoires of a model animal, the

92 eights of M-protein and therapeutic antibody light chain are conveniently used for quantitation.

93 We show that active NMII light chains are colocalized with actin rings and organi

94 a, tau, phosphorylated tau and neurofilament light chain, are likely to be relevant to other neurodeg

95 munoglobulin G (IgG) index and neurofilament light chain (area under the curve [AUC] = 0.95).

96 Light chain-associated amyloidosis is characterized by t

97 s that might serve as therapeutic agents for light chain-associated amyloidosis.

98 from baseline in CSF levels of neurofilament light chain at Week 78 (increases of 7.2 and 14.6 pg/ml

99 n of human germline immunoglobulin heavy and light chains at their endogenous loci in mice.

100 high-throughput mapping of paired heavy- and light-chain BCR sequences to their cognate antigen speci

101 onstruct and of Protein L, a human IgG kappa light chain binding protein.

102 tants demonstrated that neither the clathrin light chain-binding domain nor the clathrin heavy chain-

103 e native state to the constant domain of the light chain (C(L)).

104 and absence of a clonal immunoglobulin, and light-chain CA (AL) was diagnosed via tissue biopsy.

105 No patient with light-chain cardiac amyloidosis had positive SPECT.

106 Light chain cast nephropathy (LCCN) in multiple myeloma

107 ight chain proximal tubulopathy (n = 2), and light chain cast nephropathy (n = 1).

108 light chain proximal tubulopathy (n=2), and light chain cast nephropathy (n=1).Second, we conducted

109 Part 2: Whereas light chain cast nephropathy occurred the earliest and h

110 Paired heavy and light chain cDNAs from dominant plasmablast clones were

111 Clathrin light chain (CLC) subunits in vertebrates are encoded by

112 LatB decreased AFL1-Clathrin Light Chain colocalization, further indicating that effe

113 lammation, and reduced phosphorylated myosin light chain concentration.

114 The light chain constitutes the transport subunit whereas th

115 HCs, raising the intriguing possibility that light chains contribute to specialized myosin functions.

116 immunoglobulin isotypes; immunoglobulin free light chains; cytokines; and chemokines.

117 We previously reported a new form of light chain deposition disease (LCDD) presenting as diff

118 s (PGNMID) (n = 13), AL amyloidosis (n = 5), light chain deposition disease (n = 5), light chain prox

119 osits (PGNMID) (n=13), AL amyloidosis (n=5), light chain deposition disease (n=5), light chain proxim

120 that is found in variable domains of lambda light-chain deposits in 25% of patients.

121 Immunoglobulin light chain-derived (AL) amyloidosis is a debilitating d

122 ference between involved and uninvolved free light chains (dFLC) >50 mg/L were included in 15 centers

123 lved amyloidogenic and uninvolved serum-free light chains (dFLC) < 10 mg/L (low dFLC response) predic

124 ell dyscrasia (difference between serum free light chains [dFLC]) >180 mg/L as an overall strong nega

125 turally mimic naturally existing Bence-Jones light-chain dimers in their variable domains and remain

126 Therefore, both heavy-light chain dissociation and the deconjugation of the wa

127 determining region H3 loops but accommodates light-chain diversity.

128 Egl also interacts with Dynein light chain (Dlc) and Bicaudal-D (BicD).

129 human heavy-chain variable domain without a light-chain domain.

130 cket (purine binding loop) and the essential light chain, emphasizing an important role for this vari

131 of Bcl-2, Bax, Bcl-xL, nuclear factor kappa-light chain enhancer of activated B cells (NF-kappaB), c

132 ar translocation of the nuclear factor kappa light chain enhancer of activated B cells family member

133 ion programs, including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) ac

134 H. pylori-induced nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) ac

135 ho-signaling within the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) an

136 transcription factor nuclear factor of kappa-light-chain-enhancer of activated B cells (NF-kappaB) ar

137 minal kinase (JNK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) as

138 Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) si

139 R1) activation controls nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) si

140 Here, we identify nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB)-in

141 ranslocation, a subunit nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), respe

142 ition robustly enhances nuclear factor kappa-light-chain-enhancer of activated B cells activity and t

143 nolide, a caspase-1 and nuclear factor kappa-light-chain-enhancer of activated B cells inhibitor that

144 se pathways and reduced nuclear factor kappa-light-chain-enhancer of activated B cells signaling with

145 acetylation, NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity, VCA

146 ll undergoes NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells)-dependent inf

147 n coactivator-1, Jacob, nuclear factor kappa-light-chain-enhancer of activated B cells, RING finger p

148 of transcription 3 and nuclear factor kappa-light-chain-enhancer of activated B cells-p65, increased

149 degree of activation of nuclear factor kappa-light-chain-enhancer of activated B cells; NO generation

150 abilize NIK (NF-kappaB [nuclear factor kappa-light-chain-enhancer of activated B cells]-inducing kina

151 n maximal activation of nuclear factor kappa-light-chain-enhancer of B cells (NF-kappaB) and is essen

152 lls exhibited restricted immunoglobulin (Ig) light chain expression (either Igkappa or Iglambda), as

153 s, followed by extensive phagocytosis of the light chain fibrils by macrophages, leading to dissoluti

154 To better elucidate the phagocytosis of light chain fibrils, a potential method of cell-mediated

155 cess level of monoclonal immunoglobulin free light chains (FLCs) in the circulation; however, it is n

156 nt amounts of monoclonal immunoglobulin free light chains (FLCs).

157 of this adhesion complex and functions as a light chain for myosin-7b.

158 tion with myosin-7b, with CALML4 acting as a light chain for this myosin.

159 Here, we show that light chain formation resulting from the C-terminal clea

160 tudied the fibril structure of a recombinant light chain fragment corresponding to the fibril protein

161 4FPs) generated by mutations in the ferritin light chain (FtL) gene in HF.

162 untranslated region (5'-UTR) of the ferritin light chain (FTL) gene that cause hyperferritinemia are

163 articular, multiple studies of neurofilament light chain have highlighted its importance as a diagnos

164 amely, between adjacent heavy chains, at the light chain-heavy chain interface and within the trimeri

165 e clone with 100% paired IGH: immunoglobulin light chain (IGK) sequences.

166 he V gene region of the immunoglobulin kappa light chain (Igkappa) locus that becomes active precedin

167 (HCO-HD) can remove large quantities of free light chain immunoglobulin from serum, but its effect on

168 ast nephropathy is caused by pathogenic free light chain immunoglobulin in serum.

169 ne loss around plaque and more neurofilament light chain in CSF.

170 type, probably through editing toward lambda light chain in mature B cells.

171 Neurofilament light chain in the CSF was assessed as a biomarker of ne

172 e probes on the myosin-associated regulatory light chain in the thick filaments and on troponin C in

173 exposed humans, levels of the neurofilament light chain increase after LC-PCB exposure, indicating n

174 The N-terminal extension of one regulatory light chain interacts with the tail, and the other with

175 ells will express either immunoglobulin (Ig) light chain kappa or lambda, we designed a second-genera

176 in vivo, the precise role of cardiac myosin light chain kinase (cMLCK), the primary kinase acting up

177 l TJ permeability and the increase in myosin light chain kinase (MLCK) expression, confirming the reg

178 Myosin light chain kinase (MLCK) is a key effector of barrier d

179 trafficking, leading to activation of myosin light chain kinase (MLCK).

180 in a gene of major effect, Stretchin Myosin light chain kinase (Strn-Mlck), which we validate with l

181 s determined by increased activity of myosin light chain kinase in the cytoplasm and enhanced nuclear

182 The myosin light chain kinase long (MYLK-L) isoform is canonically

183 We reveal that the calcium-calmodulin-myosin light chain kinase pathway controls sheath contraction.

184 CaM binding domain of skeletal muscle myosin light chain kinase, forms a complex with CaM in the pres

185 nd myosin II motor-dependent (but not myosin light chain kinase-dependent) epithelial barrier regulat

186 ecule permeability but did not affect myosin light chain kinase-induced increases in epithelial barri

187 locking the nuclear factor-kappaB and myosin light chain kinase-mediated redistribution of the major

188 lly, of myosin ATPase, Rho kinase, or myosin light-chain kinase activity).

189 ic myofibroblast functions, including myosin light-chain kinase-mediated myofibroblast contractility,

190 mouse PAT1 is similar to that of the kinesin light chain (KLC), and we found that PAT1 binds to KLC d

191 reduced phosphorylation of regulatory myosin light chains known to activate this ATPase.

192 Light chain (LC) deposition disease (LCDD) is a rare dis

193 chain amyloidosis, an overexpressed antibody light chain (LC) forms fibrils which deposit in organs a

194 y chain but no drug conjugation near CDRs of light chain (Lc) from lysine conjugated T-DM1.

195 e role of the monoclonal immunoglobulin (Ig) light chain (LC) is strongly suspected because of the hi

196 was reduced to generate six unique subunits: light chain (Lc) without drug (Lc0), Lc with 1 drug (Lc1

197 In Ig light-chain (LC) amyloidosis (AL), the unique antibody L

198 Amyloid light-chain (LC) amyloidosis is a protein misfolding dis

199 Here, we focus on dynein light chain LC8 as a canonical example of dynamic hub pr

200 llar deposition of monoclonal immunoglobulin light chains (LCs) in vital organs, such as heart, is as

201 ved heavy chains (HCs) with IGLV3-21-derived light chains (LCs), and is associated with an unfavorabl

202 ions on T2-weighted MRI, serum neurofilament light chain levels at month 3, and change in brain volum

203 on T2-weighted MRI, and serum neurofilament light chain levels, but not the change in brain volume,

204 on for the MYC, BCL2, BCL6, and IG heavy and light chain loci was used, and results were correlated w

205 and, in most cases, the immunoglobulin kappa light chain locus.

206 RC26UCA heavy chain with the mouse surrogate light chain may contribute to this phenotype.

207 Further, light chain MG (LC-MG) was identified and studied in par

208 terodimeric Fc eliminates the possibility of light chain mispairing.

209 ased JNK2 phosphorylation and reduced myosin light chain (MLC(20) ) phosphorylation.

210 exhibited reduced phosphorylation of myosin light chain (MLC) and focal adhesion kinase (FAK), suppo

211 elial permeability by phosphorylating myosin light chain (MLC-P).

212 be tuned by the degree of myosin regulatory light chain (MRLC) phosphorylation, which appears to be

213 hila ortholog of nonmuscle myosin regulatory light chain (MRLC), which was necessary for transformati

214 M7.8L RNAi in 3-day-old humanized regulatory light chain mutant transgenic mice silenced the mutated

215 Myosin light chain (MYL1 and MYL3) showed high oxidative suscep

216 Two groups of myosin regulatory light chain N47K transgenic mice were injected with M7.8

217 nd controls, were analysed for neurofilament light chain (NF-L) and Olink Neurology and Inflammation

218 Neurofilaments light chain (Nf-L), an integral part of the axonal struc

219 uracy than plasma P-tau181 and neurofilament light chain (NfL) (AUC range, 0.50-0.72; P < .05).

220 omarkers, including total-tau, neurofilament light chain (NfL) and amyloid-beta, are increasingly bei

221 Establishment of neurofilament light chain (NfL) as a reliable biomarker of axonal dama

222 Plasma GFAP and neurofilament light chain (NfL) concentration were measured in 469 ind

223 Neurofilament light chain (NfL) is a neuronal cytoplasmic protein high

224 Neurofilament light chain (NfL) is a promising biomarker of active axo

225 Neurofilament light chain (NfL) is a promising blood biomarker in gene

226 Neurofilament light chain (NfL) is a promising fluid biomarker of dise

227 In different FTLD subtypes, neurofilament light chain (NfL) is a promising marker, therefore we in

228 Neurofilament light chain (NFL) measurement has been gaining strong su

229 g datasets as well as with CSF neurofilament light chain (NfL) using linear regression analyses.

230 The CSF biomarkers neurofilament light chain (NFL), S100B, glial fibrillary acidic protei

231 s a marker of neuronal damage, neurofilament light chain (NfL), using enzyme-linked immunosorbent ass

232 1-40)), total tau protein, and neurofilament light chain (NFL); tau phosphorylated at threonine 181 (

233 physin), axonal (neurofilament/neurofilament light chain [NFL]), inflammatory, and antioxidant (enzym

234 e weighted average DAR in both the heavy and light chains of a model antibody-drug conjugate, and cal

235 tly cleave disulfide bonds linking heavy and light chains of mAbs using electron capture dissociation

236 s from 384 MM patients (excluding those with light-chain-only disease) treated in the GEM2012MENOS65

237 ning CR in MM patients other than those with light-chain-only disease.

238 Partial loss of function of dynein light chain or Hook also enhanced mutant CHMP2B toxicity

239 rstitial myocardial infiltration, usually by light chains or transthyretin.

240 age enabled determination of heavy chain and light chain pairing from a single experiment and experim

241 tics is the determination of heavy chain and light chain pairing.

242 iming and the mode of recognition of its two light chains (PfELC and MTIP) by two degenerate IQ motif

243 57Arg]) affecting the same residue of myosin light chain, phosphorylatable, fast skeletal muscle (MYL

244 late blood-brain barrier function via myosin light chain phosphorylation and increase in permeability

245 t affect ACh-stimulated SM myosin regulatory light chain phosphorylation.

246 : one in invertebrates, by either regulatory light-chain phosphorylation (as in arthropods) or Ca(2+)

247 decreases PC relaxation by increasing myosin light-chain phosphorylation.

248 Confocal images of phospho-myosin light chain (pMLC) immunofluorescence, moreover, reveale

249 active RhoA and ROCK effector phospho-myosin light chain (pMLC) were downregulated in endothelial cel

250 P5K1C90 and subsequent phosphorylated myosin light chain polarization, and this polarization signalin

251 tithrombin or SerpinC, Immunoglobulin lambda light chain, Preprogehrelin, selenium binding protein 1(

252 Dephosphorylation of its regulatory light chain promotes an inactive, 'shutdown' state with

253 an adaptor to couple proteasomes with dynein light chain proteins (DYNLL1/2).

254 5), light chain deposition disease (n = 5), light chain proximal tubulopathy (n = 2), and light chai

255 (n=5), light chain deposition disease (n=5), light chain proximal tubulopathy (n=2), and light chain

256 a >=1.5 g/d, hematuria, and an elevated free light chain ratio increase the likelihood of finding MGR

257 on included the presence of an elevated free light chain ratio, proteinuria, and hematuria.

258 rate that IgCaller identifies both heavy and light chain rearrangements to provide additional informa

259 Very good partial response (free light chain reduction >= 90%) or more was achieved in 36

260 s in the proximal tubule of the kidney, free light chains, renal fibroblasts, and myeloma cells.

261 bind factor Xa and, with contributions from light chain residues in this neck region, contribute to

262 n two subjects (16 or 22% of lambda or kappa light chains, respectively, were shared by all three).

263 ty of the Ib or Is neuron with tetanus toxin light chain resulted in structural changes in muscle inn

264 fluorescent protein (EGFP)-tagged regulatory light chain (RLC) of NMII and mCherry-Actin.

265 Although myosin regulatory light chain (RLC) phosphorylation has been studied exten

266 e phosphorylation of Ser19 of the regulatory light chain (RLC).

267 Unique sets of essential and regulatory light chains (RLCs) are known to assemble with specific

268 ces and orientations from antibody heavy and light chain sequence.

269 ition studies also implicated several myosin light chain sequences located near HC796-835 as potentia

270 CR lineages, inferred from paired heavy- and light-chain sequences of rearranged Ig genes from multip

271 patients with < 50% reduction of serum free light chains (sFLCs) after 3 cycles, chemotherapy was re

272 all three) and 20 to 34% of lambda or kappa light chains shared between two subjects (16 or 22% of l

273 ofixation, as well as analyses of serum free light chains, should also be performed to identify the m

274 Serum neurofilament light chain (sNfL) and its ability to expose axonal dama

275 f the coiled coil, the motor domains and the light chains stabilize the shutdown molecule.

276 e partner head, revealing how the regulatory light chains stabilize the shutdown state in different w

277 MEDI3726 requires the combination of heavy-light chain structure and conjugated warhead to selectiv

278 Removal of the WDR60-WDR34-light chain subcomplex renders dynein-2 monomeric and re

279 ormed by two different protein components: a light chain subunit from an SLC7 family member and a hea

280 c protein assembly composed of two heavy and light chain subunits, respectively.

281 ts and does not include participation of the light chain subunits.

282 he CDRs, and asymmetry in the net heavy- and light-chain surface charges.

283 rojecting CeA neurons with the tetanus toxin light chain (TeLC) completely blocks auditory fear condi

284 nly a plasma cell clone, produces monoclonal light chains that exert organ toxicity and deposit in ti

285 osis (AL amyloidosis) is caused by misfolded light chains that form soluble toxic aggregates that dep

286 potential role of serum or CSF neurofilament light chain to differentiate bvFTD from primary psychiat

287 the enzyme to either the IgG heavy chain or light chain using a long flexible linker.

288 the full rat heavy chain variable and kappa light chain variable regions repertoire for the generati

289 We show that affinity maturation of the light-chain variable domain is important for strong bind

290 IId) and slow isoform (MHC-I) with different light-chain variants.

291 ies found in humans, and use three different light chains (VK3-20, VK1-5, and VK1-33) found among sub

292 than to wild type RAS, with a complementary light chain VL domain, caused programmed cell death (PCD

293 EVs, after coating with anti-hapten antibody light chains, was assessed in hapten-induced CHS in wild

294 We also demonstrated that the light chains were produced by an intrapulmonary B-cell c

295 capsid-antibody interactions, the heavy and light chains were sequenced and their coordinates, along

296 In a proteomics study, kinesin heavy and light chains were the only significant proteins in myotu

297 nd lower expression of phosphorylated myosin light chain, which is essential for vascular smooth musc

298 ause their transport did not require kinesin light chains, which are a typical adapter for kinesin-de

299 aive human B cells expressing immunoglobulin light chains with 5-amino acid complementarity determini

300 ion of ISD fragments from both the heavy and light chains with a higher confidence in a wide mass ran