Relevant bibliographies by topics / Transcobalamina

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Transcobalamina'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Transcobalamina"

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Ulleland, Marius, Ingar Eilertsen, Edward V. Quadros, Sheldon P. Rothenberg, Sergey N. Fedosov, Erling Sundrehagen, and Lars Örning. "Direct Assay for Cobalamin Bound to Transcobalamin (Holo-Transcobalamin) in Serum." Clinical Chemistry 48, no. 3 (March 1, 2002): 526–32. http://dx.doi.org/10.1093/clinchem/48.3.526.

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Abstract Background: Only cobalamin carried by transcobalamin (holo-transcobalamin) is available for cellular uptake and hence is physiologically relevant. However, no reliable or accurate methods for quantifying holo-transcobalamin are available. We report a novel holo-transcobalamin assay based on solid-phase capture of transcobalamin. Methods: A monoclonal antibody specific for human transcobalamin with an affinity constant >1010 L/mol was immobilized on magnetic microspheres to capture and concentrate transcobalamin. The cobalamin bound to transcobalamin was then released and assayed by a competitive binding radioassay. The quantification of holo-transcobalamin was accomplished using calibrators composed of recombinant, human holo-transcobalamin. Results: The assay was specific for holo-transcobalamin and had a detection limit of 5 pmol/L. Within-run and total imprecision (CV) was 5% and 8–9%, respectively. The working range (CV <20%) was 5–370 pmol/L. Dilutions of serum were linear in the assay range. The recovery of recombinant, human holo-transcobalamin added to serum was 93–108%. A 95% reference interval of 24–157 pmol/L was established for holo-transcobalamin in 105 healthy volunteers 20–80 years of age. For 72 of these sera, holo-haptocorrin and total cobalamin were also determined. Whereas holo-haptocorrin correlated well (r2 = 0.87) with total cobalamin, holo-transcobalamin correlated poorly (r2 = 0.23) with total cobalamin or holo-haptocorrin. Conclusions: The solid-phase capture assay provides a simple, reliable method for quantitative determination of holo-transcobalamin in serum.
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Nexo, Ebba, Anna-Lisa Christensen, Torben E. Petersen, and Sergey N. Fedosov. "Measurement of Transcobalamin by ELISA." Clinical Chemistry 46, no. 10 (October 1, 2000): 1643–49. http://dx.doi.org/10.1093/clinchem/46.10.1643.

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Abstract Background: Transcobalamin is essential for the cellular internalization of cobalamin. Methods to quantify the unsaturated protein are available, but few attempts have been made to develop methods to quantify the sum of unsaturated and cobalamin saturated transcobalamin. Methods: γ-Globulins from two polyclonal rabbit antibodies against recombinant human transcobalamin were used as capture and detection antibodies, and recombinant human transcobalamin was used as calibrator in an ELISA design. Results: The ELISA is specific for transcobalamin and has a detection limit of <1.6 pmol/L. The imprecision (CV) is 4–6% for mean concentrations of 13–70 pmol/L. The central 95% interval for serum from healthy blood donors (n = 77) was ∼600-1500 pmol/L and showed limited variation with age and sex. No correlation was observed between the marker of acute phase reaction, C-reactive protein, and transcobalamin in plasma. Conclusions: The ELISA measures total transcobalamin in serum and thus can be used for measurement of transcobalamin in patients treated with cobalamin.
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Uchiyama, Yukinobu. "Transcobalamin deficiency." SEIBUTSU BUTSURI KAGAKU 38, no. 6 (1994): 403–10. http://dx.doi.org/10.2198/sbk.38.403.

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Carmel, Ralph. "Measuring and Interpreting Holo-Transcobalamin (Holo-Transcobalamin II)." Clinical Chemistry 48, no. 3 (March 1, 2002): 407–9. http://dx.doi.org/10.1093/clinchem/48.3.407.

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NIELSEN, RIKKE, BOE SANDAHL SØRENSEN, HENRIK BIRN, ERIK ILSØ CHRISTENSEN, and EBBA NEXØ. "Transcellular Transport of Vitamin B12in LLC-PK1 Renal Proximal Tubule Cells." Journal of the American Society of Nephrology 12, no. 6 (June 2001): 1099–106. http://dx.doi.org/10.1681/asn.v1261099.

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Abstract. The transcobalamin-vitamin B12complex is responsible for the transport of B12from plasma and into the tissues. The complex is filtered in the renal glomeruli and is a high-affinity ligand for the endocytic receptor megalin expressed in the proximal tubule. This study shows by the use of the proximal tubule LLC-PK1 cell line that transcobalamin-B12is internalized by megalin-mediated endocytosis. After endocytosis and accumulation in endosomes, transcobalamin is degraded and the B12molecule is released from the cells in complex with newly synthesized proteins. The release is polarized in such a way that vitamin in the apical medium is bound to proteins with the size of haptocorrin, whereas the B12released at the basolateral side is complexed to two different proteins with the sizes of transcobalamin and haptocorrin. Furthermore, transcobalamin mRNA was identified by reverse transcription-PCR in LLC-PK1 cells and human and pig kidney, whereas haptocorrin mRNA was identified only in LLC-PK1 cells. The results strongly suggest that megalin located in the proximal tubule cells is important for receptor-mediated tubular reabsorption followed by transcellular transport and release of vitamin B12complexed to newly synthesized carrier proteins. This mechanism is likely to play a significant role in the maintenance of B12homeostasis by returning filtered B12to the pool of circulating vitamin.
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Hygum, Katrine, Dorte L. Lildballe, Eva H. Greibe, Anne L. Morkbak, Steen S. Poulsen, Boe S. Sorensen, Torben E. Petersen, and Ebba Nexo. "Mouse Transcobalamin Has Features Resembling both Human Transcobalamin and Haptocorrin." PLoS ONE 6, no. 5 (May 31, 2011): e20638. http://dx.doi.org/10.1371/journal.pone.0020638.

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Schohn, H., J. L. Guéant, M. Girr, E. Nexø, L. Baricault, A. Zweibaum, and J. P. Nicolas. "Synthesis and secretion of a cobalamin-binding protein by HT 29 cell line." Biochemical Journal 280, no. 2 (December 1, 1991): 427–30. http://dx.doi.org/10.1042/bj2800427.

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An HT 29 cell line derived from human colonic carcinoma was shown to synthesize and release a cobalamin-binding protein. The cobalamin-binding protein was classified as transcobalamin (TC). By gel filtration on Sephacryl S200 HR, we observed that the secreted protein bound to cobalamin had the same size as plasma transcobalamin. Like transcobalamin, the cobalamin-binding protein bound cobalamin but not cobinamide. Purification of the cobalamin-binding protein was performed by heparin-Sepharose affinity chromatography and by Sephacryl S200 gel filtration. The molecular mass of the purified protein was estimated at 44 kDa by SDS/PAGE. The isoelectric point was determined to be 6.4. The purified cobalamin-binding protein reacted with an antiserum produced against human transcobalamin. A 44 kDa band was also identified by SDS/PAGE of an immunoprecipitated homogenate from HT 29 cells labelled with [35S]methionine and in a Western blot of cell homogenates. The secretion of the cobalamin-binding protein was maximal between 10 and 12 days of cell culture and was inhibited by cycloheximide.
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van Asselt, Dieneke Z. B., Chris M. G. Thomas, Martin F. G. Segers, Henk J. Blom, Ron A. Wevers, and Willibrord H. L. Hoefnagels. "Cobalamin-binding proteins in normal and cobalamin-deficient older subjects." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 40, no. 1 (January 1, 2003): 65–69. http://dx.doi.org/10.1258/000456303321016187.

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Background: The causes of cobalamin (vitamin B12) deficiency in older people are only partly understood. We investigated the role of the cobalamin-binding proteins and tested the hypothesis that low saturated transcobalamin concentration is an early marker of cobalamin deficiency. Methods: We measured saturated (holo) and unsaturated (apo) transcobalamin and haptocorrin concentrations in healthy middle-aged volunteers, healthy older volunteers, cobalamin-deficient older volunteers and cobalamin-deficient older patients. Results: Holo and apo concentrations of transcobalamin and haptocorrin were similar in healthy middle-aged and older subjects. Holotranscobalamin concentrations were significantly decreased in cobalamin-deficient subjects but did not differ between healthy volunteers and patients. Furthermore, the relative amount of cobalamin on transcobalamin (i.e. holotranscobalamin/holotranscobalamin + holohaptocorrin) was similar in all four groups. Conclusions: Abnormalities of the cobalamin-binding proteins are not a cause of cobalamin deficiency in the aged. Plasma holotranscobalamin concentration did not differ between stages of cobalamin deficiency in older persons. Therefore, plasma holotranscobalamin is not an early marker of cobalamin deficiency in older people and has no additional value in the diagnostic work-up of reduced plasma cobalamin concentrations in older people.
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McCaddon, Andrew, Kaj Blennow, Peter Hudson, Alan Hughes, Joan Barber, Rob Gray, Gareth Davies, et al. "Transcobalamin Polymorphism and Serum Holo-Transcobalamin in Relation to Alzheimer’s Disease." Dementia and Geriatric Cognitive Disorders 17, no. 3 (2004): 215–21. http://dx.doi.org/10.1159/000076359.

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Abuyaman, Omar, Niels Torring, Rima Obeid, and Ebba Nexo. "First trimester serum levels of the soluble transcobalamin receptor, holo-transcobalamin, and total transcobalamin in relation to preeclampsia risk." Scandinavian Journal of Clinical and Laboratory Investigation 76, no. 8 (October 4, 2016): 641–44. http://dx.doi.org/10.1080/00365513.2016.1230885.

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Dissertations / Theses on the topic "Transcobalamina"

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Lazaro, Robson José. "Associação entre os polimorfismos nos genes da Transcobalamina II (TCN2 c.776C>G e TC2 c. 67A>G) e da metilenotetraidrofolato redutase (MTHFR c.677C>T) e o risco de ter abortos espontâneos recorrentes." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-01072015-122926/.

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O aborto espontâneo recorrente (AER) é definido pela ocorrência de três ou mais abortos espontâneos consecutivos com idade gestacional de até 20 semanas. O AER é um evento multifatorial, tem um índice de elucidação da causa na ordem de 50% e, mesmo com os avanços da medicina diagnóstica ainda assim 40% dos casos permanecem com sua causa desconhecida. O crescimento fetal é totalmente dependente do aporte de nutrientes oirundos da mãe, dentre esses nutrientes a cobalamina e o ácido fólico desempenham um papel fundamental para a viabilidade fetal. O objetivo geral deste estudo foi investigar se existe associação entre polimorfismos em genes relacionados ao metabolismo da cobalamina (MTHFR c.677C>T, TCN2 c. 776C>G e TCN2 c. 67A>G), e o aborto espontâneo recorrente. Os objetivos específicos deste estudo foram: 1 determinar se os polimorfismos MTHFR c. 677C>T, TCN2 c. 776C>G e TCN2 c. 67A>G estão associados ao aborto primário e secundário. 2 - Avaliar se os genótipos dos polimorfismos estudados estão relacionados com as concentrações séricas de cobalamina, folato e homocisteína total em mulheres com aborto espontâneo recorrente. Foram incluídas 256 mulheres com história de abortos espontâneos recorrentes, provenientes do Ambulatório de Obstetrícia da Clínica Obstétrica do Hospital das Clínicas da Faculdade de Medicina da USP e 264 mulheres saudáveis, sem história de aborto espontâneo e que tenham tido pelo menos duas gestações normais (grupo controle), pareadas segundo as idades. Foram colhidas amostras de sangue para a realização das dosagens bioquímicas, hormonais e das vitaminas e também para a realização das genotipagens dos polimorfismos por meio de PCR-RPFL (MTHFR c.677C>T , TCN c.776C>G e c. 67A>G). As dosagens bioquímicas e hormonais apresentaram resultados dentro dos limites de variação do normal. Quanto as concentrações de folato e cobalamina, houve diferença estatística significante entre os grupos p<0,05. As frequências dos genótipos e alelos para os polimorfismos estudados comparadas entre os grupos abortos primário, aborto secundário e grupo controle não apresentaram diferença estatística significante. Optamos a seguir por dividir o grupo de estudo entre abortos primários, onde não existe história de feto viável, e secundário neste caso onde há história de feto viável. Desta forma foram refeitas as análises estatísticas entre os grupos e encontramos diferença estatísticamente significante p<0,05 quando confrontamos os genótipos do polimorfismo TCN c.776C>G entre o grupo primário e o grupo controle. Em conclusão, quando comparamos as frequência dos genótipos e alelos em conjunto não apresentaram associação com o AER. Quando comparado separadamente o grupo de aborto primário e grupo controle houve diferença estatística significante associando o polimorfismo TCN2 c.776C>G ao AER primário.
The recurrent spontaneous abortion (RSA) is defined by the occurrence of three or more consecutive miscarriages with gestational age up to 20 weeks. The AER is a multifactorial event, has an index of elucidating the cause of around 50% and, even with advances in diagnostic medicine still remain 40% of cases with a known cause. Fetal growth is totally dependent on the supply of nutrients from the mother oirundos among these nutrients cobalamin and folic acid play a key role in fetal viability. The aim of this study was to investigate whether there is an association between polymorphisms in genes related to metabolism of cobalamin (MTHFR c.677C> T, c TCN2. 776c> G and c TCN2. 67A> G), and recurrent miscarriage. The specific objectives of this study were: 1 determine whether MTHFR c. 677C> T, TCN2 c. 776c> G and c TCN2. 67A> G are associated with abortion primary and secondary. 2 - Assess whether the genotypes studied polymorphisms are associated with serum concentrations of cobalamin, folate and total homocysteine in women with recurrent spontaneous abortion. We included 256 women with a history of recurrent miscarriages, from the Clinic of Gynecology, Obstetrics, Hospital das Clinicas, Faculty of Medicine, USP and 264 healthy women with no history of miscarriage and have had at least two normal pregnancies (group control), matched according to age. Blood samples were collected to perform the biochemical, hormonal and vitamins and also to perform the genotyping of polymorphisms by PCR-RPFL (MTHFR c.677C> T, TCN c.776C> G and c. 67A> G). The biochemical and hormonal results presented within the limits of normal variation. As the concentrations of folate and cobalamin, statistically significant difference between groups p <0.05. The frequencies of genotypes and alleles for the polymorphisms studied compared between groups abortions primary, secondary and abortion control group showed no statistically significant difference. We chose then to divide the study group between primary abortions where there is a history of viable fetus, and secondary in this case where there is a history of viable fetus. Thus were repeated statistical analyzes between groups and found statistically significant difference p <0.05 when confronted TCN genotypes of polymorphism c.776C> G between the primary group and the control group. In conclusion, when comparing the frequency of genotypes and alleles together apresntaram no association with AER. When compared separately the group of abortion primary and control group was statistically significant associated polymorphism TCN2 c.776C> G the primary AER.
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Schohn, Hervé. "Purification et caractérisation des protéines entérocytaires impliquées dans l'absorption de la vitamine B12 (récepteur du facteur intrinsèque et transcobalamine) dans l'intestin mature et fœtal." Nancy 1, 1990. http://www.theses.fr/1990NAN10399.

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Nous avons étudié 2 protéines impliquées dans l'absorption iléale de la vitamine B12 ou cobalamine : le récepteur du complexe facteur intrinsèque-cobalamine et la transcobalamine. Le récepteur du complexe facteur intrinsèque-cobalamine est exprimé dès la dixième semaine du développement fœtal chez l'homme. Le récepteur iléal porcin a été purifié par chromatographie d'affinité sur un support sépharose-facteur intrinsèque. Il se compose de 4 polypeptides dont trois sont glycosyles. La liaison entre le récepteur et son ligand peut être inhibé en présence d'agglutinine de germe de blé. L'inhibition est due à la fixation de cette lectine à la sous-unité alpha du récepteur qui contient le site de fixation du complexe facteur intrinsèque-cobalamine. Les résidus galactosyls de la copule glucidique du facteur sont importants dans la formation de la liaison entre le récepteur et son ligand. Enfin, nous avons montré l'existence de la synthèse et de la sécrétion de transcobalamine par les cellules HT 29. Ces cellules ont été stabilisées à partir d'un carcinome colique et représentent un modèle entérocytaire in vitro
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Semmler, Alexander, Michael Linnebank, Dietmar Krex, Anika Götz, Susanna Moskau, Andreas Ziegler, and Matthias Simon. "Polymorphisms of Homocysteine Metabolism Are Associated with Intracranial Aneurysms." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135282.

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Background: Impaired homocysteine metabolism is associated with a number of vasculopathies including extracranial aneurysms. We analyzed the possible association of nine genetic variants of homocysteine metabolism with the occurrence of intracranial aneurysms. Methods: Caucasian patients (n = 255) treated at two German hospitals for intracranial aneurysms and local controls (n = 348) were genotyped for the following polymorphisms: methionine synthase (MTR) c.2756A→G, methylenetetrahydrofolate reductase (MTHFR) c.677C→T, MTHFR c.1298A→C, cystathionine β-synthase (CBS) c.844_855ins68, CBS c.833T→C, dihydrofolate reductase (DHFR) c.594 + 59del19bp, glutathione S-transferase Ω-1 (GSTO1) c.428C→A, reduced folate carrier 1 (RFC1) c.80G→A and transcobalamin 2 (Tc2) c.776C→G. Results: The G-allele of the missense polymorphism Tc2 c.777C→G was found to be underrepresented in patients, suggesting that this variant may protect from the formation of cerebral aneurysms [odds ratio per two risk alleles (OR) 0.48; 95% confidence interval (CI) 0.30–0.77; p = 0.002]. We obtained borderline results for the G-allele of RFC1 c.80G→A (OR 1.64; 95% CI 1.01–2.65; p = 0.051) and the insertion allele of DHFR c.594 + 59del19bp (OR 1.61; 95% CI 1.00–2.60; p = 0.059), which were found to be overrepresented in patients. Conclusion: Polymorphisms of homocysteine metabolism are possible risk factors for the formation of intracranial aneurysms
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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Yamani, Lama. "Studies on transcobalamin in cultured fibroblasts from patients with inborn errors of cobalamin metabolism." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112320.

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Cobalamin must be metabolized intracellularly in order to bind two enzymes: methionine synthase in cytoplasm and methylmalonyl-CoA mutase in mitochondria. Defects in this process cause different inborn errors of cobalamin metabolism (cblA-cblG and mut). A previous study described a cobalamin-binding protein, in addition to methylmalonyl-CoA mutase, in crude mitochondrial fractions. The amount of [57Co]cobalamin bound to this protein was increased in cblB, mut and cblD variant2 cell lines, compared to control cell lines. In the present study, this protein was identified as transcobalamin (TC). Mitochondrial fractions from a cblB cell line were incubated with anti-TC antibodies, which precipitated the cobalamin-bound protein. Analysis of mitochondrial and cytoplasmic fractions isolated from a chloroquine-incubated cblF cell line showed that isolated mitochondrial fractions contain lysosomal material, suggesting that the identified TC is lysosomal. Quantification of cobalamin-bound TC levels in whole cell extracts showed significant increases in cblB and mut groups compared to control cell lines.
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Semmler, Alexander, Michael Linnebank, Dietmar Krex, Anika Götz, Susanna Moskau, Andreas Ziegler, and Matthias Simon. "Polymorphisms of Homocysteine Metabolism Are Associated with Intracranial Aneurysms." Karger, 2008. https://tud.qucosa.de/id/qucosa%3A27635.

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Background: Impaired homocysteine metabolism is associated with a number of vasculopathies including extracranial aneurysms. We analyzed the possible association of nine genetic variants of homocysteine metabolism with the occurrence of intracranial aneurysms. Methods: Caucasian patients (n = 255) treated at two German hospitals for intracranial aneurysms and local controls (n = 348) were genotyped for the following polymorphisms: methionine synthase (MTR) c.2756A→G, methylenetetrahydrofolate reductase (MTHFR) c.677C→T, MTHFR c.1298A→C, cystathionine β-synthase (CBS) c.844_855ins68, CBS c.833T→C, dihydrofolate reductase (DHFR) c.594 + 59del19bp, glutathione S-transferase Ω-1 (GSTO1) c.428C→A, reduced folate carrier 1 (RFC1) c.80G→A and transcobalamin 2 (Tc2) c.776C→G. Results: The G-allele of the missense polymorphism Tc2 c.777C→G was found to be underrepresented in patients, suggesting that this variant may protect from the formation of cerebral aneurysms [odds ratio per two risk alleles (OR) 0.48; 95% confidence interval (CI) 0.30–0.77; p = 0.002]. We obtained borderline results for the G-allele of RFC1 c.80G→A (OR 1.64; 95% CI 1.01–2.65; p = 0.051) and the insertion allele of DHFR c.594 + 59del19bp (OR 1.61; 95% CI 1.00–2.60; p = 0.059), which were found to be overrepresented in patients. Conclusion: Polymorphisms of homocysteine metabolism are possible risk factors for the formation of intracranial aneurysms.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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Namour, Bernard. "Phénotypes et concentrations relatives des isoprotéines de la transcobalamine II rapportés au polymorphisme Arg/Pro du codon 259." Nancy 1, 1999. http://www.theses.fr/1999NAN19901.

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Boukhzer, El Bachir. "Caractérisation d'un récepteur membranaire de la transcobalamine II au niveau des cellules de la ligne germinale mâle du lapin." Nancy 1, 1995. http://docnum.univ-lorraine.fr/public/SCD_T_1995_0447_BOUKHZER.pdf.

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Dans les années 60 Sharp et Witts, Watson et Morales, ainsi que Griswold démontrent que la vitamine B 12 influence la spermatogenèse. Les stérilités observées, chez les patients des deux sexes atteints d'anémie pernicieuse, peuvent être surmontées par une thérapie à la vitamine B12. L'aspect biochimique de cette stérilité, les cellules cibles concernées et le rôle joué par la vitamine B12 , demeurèrent inconnues. Le but de cette étude a été de rechercher et de caractériser le récepteur du complexe transcobalamine-vitamine B12 au niveau des cellules germinales mâles. La présence de récepteurs de transcobalamine-vitamine B 12 au niveau des cellules germinales mâles souligne l'importance de la vitamine B12 comme nutriment indispensable au métabolisme des cellules germinales et à leur maturation.
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Hannibal, Luciana. "Intracellular Processing of Cobalamins in Mammalian Cells." Kent State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=kent1247938485.

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Schrempf, Robert [Verfasser]. "Stoffwechselaktives, Transcobalamin-II-gebundenes Vitamin B12 im Vergleich zum gesamten Vitamin B12 : ein neuer Labortest / vorgelegt von Robert Schrempf." 2004. http://d-nb.info/973286288/34.

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Book chapters on the topic "Transcobalamina"

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Hitzig, W. H., Marijke Fràter-Schröder, and R. Seger. "Immunodeficiency Due to Transcobalamin II Deficiency." In Ciba Foundation Symposium 68 - Enzyme Defects and Immune Dysfunction, 77–99. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720516.ch6.

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Adkins, Yuriko, and Bo Lönnerdal. "Binding of Transcobalamin II by Human Mammary Epithelial Cells." In Advances in Experimental Medicine and Biology, 469–77. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1371-1_58.

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Hassan, Ian F., Ian J. Parsons, and Martin W. Mackay. "Receptor-Mediated Transport of Cobalamin in Caco-2 Cells: Intracellular Localisation of Transcobalamin II." In Pharmaceutical Applications of Cell and Tissue Culture to Drug Transport, 107–20. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4757-0286-6_9.

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Rodan, Lance Harrington, Navin Mishra, Ivanna Yau, Andrea Andrade, Komudi Siriwardena, and Ingrid Tein. "Expanding the Spectrum of Methylmalonic Acid-Induced Pallidal Stroke: First Reported Case of Metabolic Globus Pallidus Stroke in Transcobalamin II Deficiency." In JIMD Reports, 7–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/8904_2013_215.

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"Transcobalamin." In Springer Reference Medizin, 2333. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_313712.

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"Transcobalamin (TCN1)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1989. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_17182.

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"Transcobalamin (TC2)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1989. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_17183.

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"TCN2: Transcobalamin II." In Encyclopedia of Medical Immunology, 634. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_300345.

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Seetharam, Bellur, and Ning Li. "Transcobalamin II and its cell surface receptor." In Vitamins & Hormones, 337–66. Elsevier, 2000. http://dx.doi.org/10.1016/s0083-6729(00)59012-8.

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Rothenberg, Sheldon P., and Edward V. Quadros. "Quantitative methods for measurement of transcobalamin II." In Methods in Enzymology, 261–68. Elsevier, 1997. http://dx.doi.org/10.1016/s0076-6879(97)81032-4.

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