The Proteins of Transport of the Cobalamins

Hall, Charles A.

doi:10.1007/978-3-642-74364-1_4

Cited by 4 publications

(6 citation statements)

References 47 publications

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“…Burger et al(19 7 5) showed that the liver of the rabbit took up Hc-Cbl by the receptor system responsive to asialoglycoproteins in general. Whereas we observed the uptake of Hc-Cbl by human hepatocytes to be inefficient as compared to uptake by the receptor system for TCII and subject to other limiting factors, Hc-Cbl can enter hepatocytes (Hall et al, 1989). Possibly through the combination of retained Cbl, small amounts of Cbl uptake from Hc and betaine dependent Met synthesis, enough Met can be supplied by the liver to protect the CNS.…”

Section: Discussionmentioning

confidence: 63%

“…The present analysis is based on 36 cases of the genotype TC2*SEA/TC2*SEA (Hall, 1989) known to the author. Thirteen cases have been published as full papers and two cases as abstracts.…”

Section: Patient Population and Methodsmentioning

confidence: 99%

“…TCII is a trace protein in plasma that binds Cbl as it is released from intrinsic factor within the enterocyte and binds Cbl released by tissues as it recycles, although it is not known whether this recycled Cbl binds to TCII within cells or in the circulation (Fig 1). TCII-Cbl is taken up by specific, high affinity receptors which have been observed in several human cells and this process is the means by which all tissues studied to date obtain their Cbl (Hall, 1989). Therefore, the individual with an inherited inability to synthesize a functional TCII cannot absorb Cbl nor transfer it into tissues and has.…”

mentioning

confidence: 99%

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The neurologic aspects of transcobalamin II deficiency

Hall

1992

Br J Haematol

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Thirty-four symptomatic cases of inherited transcobalamin II (TCII) deficiency were analysed in order to determine the frequency and nature of neurologic manifestations. In no instance was there definite evidence of a neurologic disorder at the time of presentation as a young infant. One child of 2 1/2 years transiently lost deep tendon reflexes at a time of suboptimal treatment. A syndrome of mental retardation and other neurologic manifestations was observed in three cases, all with the following in common: (1) an extended duration of illness of 2-17 years; (2) inadequate or not treatment with Cbl; (3) treatment with folic of folinic acid. TCII deficiency rarely if ever presents with neurologic manifestations. However, neurologic disorders can be produced subsequently by improper treatment.

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Section: Discussionmentioning

confidence: 63%

“…The present analysis is based on 36 cases of the genotype TC2*SEA/TC2*SEA (Hall, 1989) known to the author. Thirteen cases have been published as full papers and two cases as abstracts.…”

Section: Patient Population and Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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The neurologic aspects of transcobalamin II deficiency

Hall

1992

Br J Haematol

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“…In comparison, a 'voidvolume' peak, referred to as 'TCo', an 'HC' peak and a very small peak corresponding to TC were observed when either concentrated culture medium or FCS was submitted to gel filtration. The 'TCO' peak may consist of aggregates of TC and HC (Carmel, 1979;Hall, 1988). A low level of TC in foetal serum has been reported previously in the serum of 20-week human foetus (Sonnenborn & Iwanik, 1974, Hansen etal., 1989.…”

Section: Resultsmentioning

confidence: 78%

Synthesis and secretion of a cobalamin-binding protein by HT 29 cell line

Schohn

Guéant

Girr

et al. 1991

Biochemical Journal

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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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“…In any case, we noted that the blood levels of HC in MH or cirrhosis are only slightly increased compared to those observed in the myeloproliferative syndrome [25].…”

Section: Discussionmentioning

confidence: 86%

Blood Transcobalamin Levels in Malignant Hepatoma

Frémont¹,

Champigneulle²,

Gérard³

et al. 1991

Tumor Biol

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α-Fetoprotein (AFP) levels measured by RIA show a strong sensitivity for the biological diagnosis of malignant hepatoma (MH). However, this parameter lacks specificity. Previous observations of an alteration in vitamin B₁₂etabolism in the presence of hepatoma led us to study vitamin-B₁₂-binding proteins. Vitamin B₁₂, also called cobalamin, is transported in the blood by two proteins or transcobalamins: one is haptocorrin (HC), which is linked to most of the cobalamin, and the other is transcobalamin II, which is involved in tissue exchanges. In this work, the levels of AFP and transcobalamins were determined by RIA and radioisotope dilution assay, respectively. They were measured in patients with MH (group A) and in patients with other liver diseases (group B). Compared with group B, group A showed a significant increase in total serum HC (p < 0.005). In conclusion, it was observed that MH is accompanied by increased levels of HC. The origin of these changes could be due to either an increase in HC synthesis or a catabolic defect.

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The Proteins of Transport of the Cobalamins

Cited by 4 publications

References 47 publications

The neurologic aspects of transcobalamin II deficiency

The neurologic aspects of transcobalamin II deficiency

Synthesis and secretion of a cobalamin-binding protein by HT 29 cell line

Blood Transcobalamin Levels in Malignant Hepatoma

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