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Chemical Compound Review

CDR     (2R,5S,6R)-6-methyloxane-2,5- diol

Synonyms: AC1NRAI9, 7358-EP2280282A1, 7358-EP2314571A2, 7358-EP2371799A1
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Disease relevance of CDR

  • Positive selection of CD34+ cells resulted in 2.5- to 3-log depletion of plasma cells and CD19+ B-lineage cells as determined by immunofluorescence studies, although DNA analysis of CDR III region of IgH gene showed the persistence of minimal residual disease in 5 of 6 patient samples studied [1].
  • All had detectable lymphoma cells before relapse and the sequence of the CDR III region at the time of relapse was identical to that obtained at the time of ABMT [2].
  • In contrast, the sequence from the follicular lymphoma showed 29 nucleotide changes giving rise to 14 amino acid substitutions, which were scattered among the CDR and FW regions [3].
  • Time-dependent phrenic motor responses to hypoxia were compared among CDR, sham-operated, and control rats [4].
  • Four rounds of selection of the phage Ab libraries on immobilized IL-1 beta gave predominantly the wild-type sequence, indicating efficient affinity maturation of this CDR in vivo [5].

Psychiatry related information on CDR

  • Those preparations that expressed the shared Id with anti-Leu 3a have virtually identical V[kappa] sequences, with a high degree of homology in the CDR [6].
  • Dementia was diagnosed according to DSM-III-R and measured by the Clinical Dementia Rating scale; CDR scores of 0, 0.5, and > or = 1, represent individuals with no dementia (n = 122), possible dementia (n = 29), and definite dementia (n = 43), respectively [7].
  • We have focused on the relationships between critical biomarkers such as tau and Abeta in the CSF and the cognitive impairment of patients, as assessed by a battery of neuropsychological tests derived from CDR and CERAD, of value in the evaluation of AD patients [8].
  • Temporal cortical sections from postmortem brains of individuals without any dementing condition and with different degrees of severity of Alzheimer's disease (AD) evaluated by the Clinical Dementia Rating scale (CDR 0-CDR 3) were analyzed using immunohistochemical procedures [9].
  • 4. The CDR is insensitive to mild psychopathology in this population [10].

High impact information on CDR

  • A key feature of the antibody-combining site is the protruding, finger-like long CDR H3 that can penetrate the recessed CD4-binding site of gp120 [11].
  • Expression of conformationally constrained adhesion peptide in an antibody CDR loop and inhibition of natural killer cell cytotoxic activity by an antibody antigenized with the RGD motif [12].
  • Patterns of sequence similarities or identities indicate recombination or gene conversion events; sets of direct and inverted repeats flank the sites of, or lie within FR or CDR sequences where these genetic events may occur [13].
  • The structure provides a rationale for mutagenesis experiments that have resulted in BR96 CDR loop mutants with increased affinity for nLey and/or tumour cells [14].
  • Three hydrogen-bond donors appear to stabilize the charged phosphonate group of the hapten: two NH groups of the heavy (H) chain complementarity-determining region 3 (H3 CDR) polypeptide chain and the side-chain of histidine-H35 in the H chain (His-H35) in the H1 CDR [15].

Chemical compound and disease context of CDR


Biological context of CDR

  • Southern blot analysis was consistent with single-copy representation of the CDR (cerebellar degeneration-related) gene in the human and mouse genome [17].
  • The finding that nucleotide segments present in a D minigene can appear in CDR2 raises the possibility that other minigene segments may be involved in the generation of antibody diversity and complementarity or that nucleotide segments may move from one CDR to another by a gene conversion mechanism [18].
  • For an epitope that is sequence-specific (anti-FIPV system), molecular mimicry appears to be present as evidenced by the sequence homology between the CDR loops of the anti-id and the epitope of the original antigen [19].
  • The three-dimensional structure of the Fv-region of the anti-DNA antibody (D42) was modeled by computer and a stretch of poly(dT), ssDNA was docked to a cleft in the antibody combining site, formed by the three H chain CDR and by CDR1 and CDR3 of the L chain [20].
  • According to the amino acid sequences of CDR 1, 2, and 3 of the mAb M7-625 variable region, there exists a homology of amino acid sequences between CDR2 in the H chain (5 amino acids of 10) and CDR3 in the L chain (3 amino acids of 9) of mAb M7-625 and domain III of CEA (545-554) [21].

Anatomical context of CDR

  • Expression of the CDR message was also noted in cell lines derived from cancers of neuroectodermal, kidney, and lung origin [17].
  • In B-cell non-Hodgkin's lymphoma (NHL), as in other B-cell malignancies, clonal rearrangement of the third complementarity determining region (CDR III) of the immunoglobulin heavy chain gene (IgH) provides a useful marker for the detection of minimal residual disease (MRD) after treatment [2].
  • The number of serotonin-immunoreactive terminals within 5 micrometer of labeled phrenic motoneuron soma and primary dendrites increased 2.1-fold after CDR versus sham-operation [4].
  • We have also cloned a counterpart Ig VL germ-line gene (SG3) from purified neutrophils of the patient and found the presence of replacement mutations only in the CDR of SC17 [22].
  • To demonstrate directly the effect of somatic mutation on Sm binding, we have engineered the unmutated counterpart of Ab 2-12, an Sm-specific hybridoma Ab with a nonrandom distribution of V kappa CDR R mutations, and compared its ability to bind Sm and ssDNA with that of the originally isolated 2-12 Ab [23].

Associations of CDR with other chemical compounds

  • Northern blotting analysis was used to monitor the expression of genes encoding lanosterol demethylase (ERG11) and efflux transporters (CDR and MDR1) in matched sets of C. dubliniensis-susceptible and -resistant isolates by using probes generated from their homologous C. albicans sequences [24].
  • Two potential alternative orientations of the A-ring, one close to CDR H3 and L2 loops, and the other one close to CDR H2 and L3 loops, have been considered for the docking of estradiol, none of which could be unambiguously privileged taking into account data from cross-reactivity measurements, photolabelling and mutagenesis studies [25].
  • No changes in activities of guanylate cyclase or in high Km cyclic AMP phosphodiesterase (with or without the calcium-dependent regulator protein, calmodulin or CDR) were observed between the control and isolated caudate [26].
  • Competitive ELISA analysis indicated that no framework changes were required in the humanized variable regions for retention of high affinity binding to C5, even at framework positions predicted by computer modeling to influence CDR canonical structure [27].
  • Site-directed mutagenesis of tyrosine residues in CDR H3 did not result in improved affinity for paraquat, suggesting that the original pH dependence required re-examination [28].

Gene context of CDR

  • B-CLL V(H) mutations concentrated in complementarity-determining region 1 (CDR1) and CDR2, which exhibited higher replacement-to-silent ratios (CDR R/S, 4.60; framework region [FR] R/S, 1.72) [29].
  • The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1 [30].
  • In the t(8;21) translocation associated with acute myeloid leukemia (AML), the AML1(CBFA2/PEBP2alphaB) gene is juxtaposed to the MTG8(ETO/CDR) gene [30].
  • Subcellular localization of the oncoprotein MTG8 (CDR/ETO) in neural cells [31].
  • This modeling indicates (1) that internal Type 3-specific residues combine to pack into a compact immunoglobulin core that supports the CDR loop regions, and (2) that despite apparent low-sequence variability, there is sufficient plasticity in the CDR3 loop to form a conformationally diverse antigen-binding surface [32].

Analytical, diagnostic and therapeutic context of CDR

  • V H sequence analyses of 36 pFv-binding antibodies revealed that binding did not correlate with CDR sequence, JH, or L chain usage [33].
  • Multiple sequence alignments have been made based on structural information; they indicate that there will be only a limited number of canonical conformations for the first and second CDR loops [34].
  • We conclude that sequencing and the use of patient specific IgH CDR III oligonucleotides probes provides a simple and highly reliable method to determine the specificity of the IgH PCR technique [2].
  • We tested the hypothesis that spinal plasticity elicited by chronic bilateral cervical dorsal rhizotomy (C3-C5; CDR) has functional implications for respiratory motor control [4].
  • Electron microscopy of immune complexes composed of rabbit Fab anti-a1 and goat Ab2 reveals that the Fab anti-a1 binds to the side of the variable region of most goat Ab2 molecules, rather than at the tip (i.e. in the CDR) as expected [35].


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  12. Expression of conformationally constrained adhesion peptide in an antibody CDR loop and inhibition of natural killer cell cytotoxic activity by an antibody antigenized with the RGD motif. Zanetti, M., Filaci, G., Lee, R.H., del Guercio, P., Rossi, F., Bacchetta, R., Stevenson, F., Barnaba, V., Billetta, R. EMBO J. (1993) [Pubmed]
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  15. Crystal structure of the complex of a catalytic antibody Fab fragment with a transition state analog: structural similarities in esterase-like catalytic antibodies. Charbonnier, J.B., Carpenter, E., Gigant, B., Golinelli-Pimpaneau, B., Eshhar, Z., Green, B.S., Knossow, M. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
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