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1 minating between benign and pathologic human immunoglobulin light chains.
2 fibrils in patients overproducing monoclonal immunoglobulin light chains.
3 -threatening disease caused by deposition of immunoglobulin light chains.
4 free kappa (kappa) and free lambda (lambda) immunoglobulin light chains.
5 nd trafficking of other glycoproteins, or of immunoglobulin light chains.
6 n of amyloid fibrils derived from monoclonal immunoglobulin light chains.
7 idosis is characterized by the misfolding of immunoglobulin light chains, accumulating as amyloid fib
13 outcome were determined for 80 patients with immunoglobulin light chain (AL) amyloidosis treated with
19 of the 2 main types of cardiac amyloidosis, immunoglobulin light chain (AL) and transthyretin (ATTR)
20 nance (CMR) between transthyretin (ATTR) and immunoglobulin light chain (AL) cardiac amyloidosis (CA)
24 and limited therapeutic options characterize immunoglobulin light-chain (AL) amyloidosis with major h
25 lignant diseases like multiple myeloma (MM), immunoglobulin light-chain (AL) amyloidosis, and monoclo
26 e kidney is involved in 70% of patients with immunoglobulin light-chain (AL) amyloidosis, but little
29 uding heart involvement of either monoclonal immunoglobulin light-chain (AL) or transthyretin (ATTR)
33 chapter "The Structural Determinants of the Immunoglobulin Light Chain Amyloid Aggregation", publish
34 that can infiltrate the heart are monoclonal immunoglobulin light-chain amyloid and transthyretin amy
43 most frequent forms of cardiac amyloidosis: immunoglobulin light chain amyloidosis and transthyretin
44 d prioritized cardiac end points relevant to immunoglobulin light chain amyloidosis in the context of
51 is study, we address the structural basis of immunoglobulin light chain amyloidosis, which results fr
54 000 and 2021, and 2 cohorts of patients with immunoglobulin light-chain amyloidosis (AL) and transthy
58 es has increased the number of patients with immunoglobulin light-chain amyloidosis receiving kidney
59 mes after kidney transplant in patients with immunoglobulin light-chain amyloidosis seem acceptable i
60 mparisons were made with other patients with immunoglobulin light-chain amyloidosis who did not have
62 al lymphoplasmacytic malignancies, including immunoglobulin light-chain amyloidosis, multiple myeloma
65 transcribed double-stranded (ds) DNA during immunoglobulin light chain and heavy chain class switch
67 is a lethal disease characterized by excess immunoglobulin light chains and light chain fragments co
68 ment of B cells that coexpress two different immunoglobulin light chains and, therefore, two antibody
69 nal B-cell disorders producing amyloidogenic immunoglobulin light chains, and the hereditary and "sen
70 is characterized by pathologic deposition of immunoglobulin light chains as amyloid fibrils in vital
72 y probabilities of selected positions of the immunoglobulin light chain-binding domain of protein L,
73 l surface and did not efficiently bind kappa immunoglobulin light chains, but did associate with Ig a
75 rimary (light chain-associated) amyloidosis, immunoglobulin light chains deposit as amyloid fibrils i
78 lls expressing CRBN, causing accumulation of immunoglobulin light-chain dimers, significantly increas
80 ta consist of 209 proteins of human antibody immunoglobulin light chains, each represented by aligned
81 BCR knock-in mice lacking self-Thy-1 ligand, immunoglobulin light chain editing occurred, generating
83 L transgene under the control of the 3'kappa immunoglobulin light chain enhancer, which is most activ
84 unction as transcriptional activators of the immunoglobulin light-chain enhancer E lambda 2.4 when co
85 Serum amyloid P component, apolipoprotein E, immunoglobulin light chains, Factor X, and complement pr
86 n amyloidosis is a devastating disease where immunoglobulin light chains form amyloid fibrils, result
89 hological deposition of insoluble fibrils of immunoglobulin light chain fragments in various tissues,
90 hological deposition of insoluble fibrils of immunoglobulin light-chain fragments in various organs a
91 ain gene segments as substrate for secondary immunoglobulin light chain gene rearrangement and is ind
93 for the ability of BCR ligation to stimulate immunoglobulin light chain gene rearrangements in immatu
94 the Fraction C'-D transition is critical for immunoglobulin light chain gene recombination and to pre
95 at is recruited to composite elements within immunoglobulin light-chain gene enhancers through a spec
96 hocyte developmental checkpoints inasmuch as immunoglobulin light-chain gene rearrangement occurred i
102 ing the immunoglobulin heavy chain (Igh) and immunoglobulin light chain (Igk) takes place sequentiall
104 Mass spectrometric analysis identified an immunoglobulin light chain in the band but found no PrP
106 presence of monoclonal free kappa or lambda immunoglobulin light chains in monoclonal gammopathy of
107 at increased monoclonal free kappa or lambda immunoglobulin light chains in smoldering multiple myelo
108 characterized by the deposition of monotypic immunoglobulin light chains in the kidney, resulting in
110 lization and cellular trafficking of urinary immunoglobulin light chains into cardiac fibroblasts.
112 ains produced by subclones stemming from one immunoglobulin light chain lambda or kappa rearrangement
113 w BiP interacts with a particular substrate, immunoglobulin light chain (lambda LC), during its foldi
121 used by the clonal production of an unstable immunoglobulin light chain (LC), which affects organ fun
122 n both AL and multiple myeloma (MM), soluble immunoglobulin light chains (LC) are produced by clonal
123 crasia characterized by clonal production of immunoglobulin light chains (LC) resulting in the subseq
126 s from overproduction of unstable monoclonal immunoglobulin light chains (LCs) and the deposition of
127 In multiple myeloma diseases, monoclonal immunoglobulin light chains (LCs) are abundantly produce
128 sis (AL), fibrillar deposition of monoclonal immunoglobulin light chains (LCs) in vital organs, such
132 idosis and familial amyloid polyneuropathy), immunoglobulin light chains (light-chain amyloid), beta2
134 e, can also lead to allelic inclusion at the immunoglobulin light chain loci and the development of B
136 center B cells, demonstrating that the kappa immunoglobulin light-chain locus becomes a substrate for
137 ens and cytokines in regulation of the kappa immunoglobulin light-chain locus, we have characterized
138 protein misfolding disease where monoclonal immunoglobulin light chains misfold and deposit as amylo
139 oidosis (AL) is a fatal disorder wherein the immunoglobulin light chain misfolds and aggregates, lead
141 arge membrane pores and high permeability to immunoglobulin light chains) or a conventional high-flux
143 izing and destabilizing mutations is key for immunoglobulin light-chains populating unfolded intermed
144 idosis, amyloid fibril deposits derived from immunoglobulin light chains produced by a clonal plasma
145 in conformation disorder in which monoclonal immunoglobulin light chains produced by clonal plasma ce
146 s element has considerable homology to mouse immunoglobulin light chain promoter sequences to which t
147 ed that the dimer interface of amyloidogenic immunoglobulin light chain protein AL-09 is twisted 90 d
148 ated with the overproduction of a monoclonal immunoglobulin light chain protein by a B-lymphocyte clo
149 minor fibril polymorph of a human lambda-III immunoglobulin light chain protein that escaped detectio
150 egulatory factor 4 (IRF-4) and IRF-8 promote immunoglobulin light-chain rearrangement and transcripti
152 t with aberrant VJ recombination between the immunoglobulin light chain region (Ig kappa) on chromoso
154 t remains tightly bound to newly synthesized immunoglobulin light chains, resulting in retention of l
156 idosis is a protein misfolding disease where immunoglobulin light chains sample partially folded stat
157 ted with amyloid fibril formation, including immunoglobulin light chain, serum amyloid A protein, and
158 631 substitutions present in 90 nurse shark immunoglobulin light chain somatic mutants, 338 constitu
160 e B cells within the HL cell lines expressed immunoglobulin light chain, the memory B-cell antigen CD
162 exchange rates) and the propensity of human immunoglobulin light chains to form amyloid fibrils in v
163 ted an FcgammaRIIB-independent difference in immunoglobulin light-chain usage, consistent with an alt
165 re we identify the monomeric form of the Mcg immunoglobulin light chain variable domain as the quater
167 loid fibrils were investigated for a dimeric immunoglobulin light chain variable domain, employing pr
169 temic extracellular deposition of monoclonal immunoglobulin light chain variable domains in the form
170 This study characterizes the repertoire of immunoglobulin light chain variable genes used by the cl
171 tional dynamics of a pathogenic kappa4 human immunoglobulin light-chain variable domain, SMA, associa
172 model for the assembly of amyloid fibrils of immunoglobulin light-chain variable domains is proposed
173 s the free light-chain assay and the role of immunoglobulin light-chain variable region germline gene
174 The structure of a multisubunit protein (immunoglobulin light chain) was solved in three crystal
175 ia characterized by misfolding of monoclonal immunoglobulin light chains which leads to aggregation a
176 ubiquitylation sites on the NS-1 nonsecreted immunoglobulin light chain, which is an ERAD substrate.
177 t selects for naive human B cells expressing immunoglobulin light chains with 5-amino acid complement