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CLTB  -  clathrin, light chain B

Homo sapiens

Synonyms: Clathrin light chain B, Lcb
 
 
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High impact information on CLTB

  • In contrast, clathrin light chain genes (CLTA and CLTB) apparently arose by localized duplication, within 1-11 million years of CHC gene duplication [1].
  • The rapid elimination of CPE-C by deamination in the primate resulted in a much higher CLTB and considerably lower total drug exposure than in rodents and dogs that clear CPE-C at a much lower rate by renal excretion [2].
  • A regional advantage for IA cisplatin and FUDR can be calculated based on total body clearance rates (CLTB) for these agents and estimates of external carotid artery (ECA) blood flow [3].
  • We also observe activity-dependent changes in alternative splicing of the clathrin light chain B, c-src and NMDAR1 genes, indicating that the coordinated change of alternative splicing patterns might contribute to molecular plasticity in the brain [4].
  • The mean (s.d.) CLTB for UPt was 281 +/- 21 ml min-1 and correlated with glomerular filtration rate (r = 0.61, P = 0.03) [5].
 

Biological context of CLTB

  • The gene (CLTA) encoding the LCa light chain maps to the long arm of chromosome 12 at 12q23-q24 and that encoding the LCb light chain (CLTB) maps to the long arm of chromosome 4 at 4q2-q3 [6].
  • Plasma carboplatin elimination (t1/2 lambda 1, 0.50 hr; t1/2 lambda 2, 2.2 hr) and CLTB (4.4 to 5.6 L/m2/hr) were also independent of dose; AUC and Cmax increased proportionally to dose [7].
 

Anatomical context of CLTB

 

Associations of CLTB with chemical compounds

  • Total plasma platinum, which represented free carboplatin, protein-bound platinum and metabolites, declined triexponentially; plasma half-lives (t1/2 lambda 1, 0.2 to 0.4 hr; t1/2 lambda 2, 1.3 to 1.7 hr; t1/2 lambda 3, 22 to 40 hr) and total body clearance (CLTB 2.8 +/- 0.5 L/m2/hr) were dose independent [7].
  • Non-compartmental PK analysis has been applied to 5-FU and 5-FUH2 concentrations, estimating the following parameters (median values): Cmax 55.44 and 6.23 microg ml(-1), respectively, AUC(0-2 h) 11.59 and 5.94 hx microg ml(-1), CLTB 30.64 and 51.81 lh(-1) m(-2), 5-FUH2/5-FU AUC ratio 0.47 (range 0.29-1.12) [9].

References

  1. Clathrin heavy and light chain isoforms originated by independent mechanisms of gene duplication during chordate evolution. Wakeham, D.E., Abi-Rached, L., Towler, M.C., Wilbur, J.D., Parham, P., Brodsky, F.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  2. Pharmacokinetics and metabolism of cyclopentenyl cytosine in nonhuman primates. Blaney, S.M., Balis, F.M., Hegedus, L., Heideman, R.L., McCully, C., Murphy, R.F., Kelley, J.A., Poplack, D.G. Cancer Res. (1990) [Pubmed]
  3. Intra-arterial cisplatin and FUDR in advanced malignancies confined to the head and neck. Forastiere, A.A., Baker, S.R., Wheeler, R., Medvec, B.R. J. Clin. Oncol. (1987) [Pubmed]
  4. Activity-dependent regulation of alternative splicing patterns in the rat brain. Daoud, R., Da Penha Berzaghi, M., Siedler, F., Hübener, M., Stamm, S. Eur. J. Neurosci. (1999) [Pubmed]
  5. Continuous carboplatin infusion during 6 weeks' radiotherapy in locally inoperable non-small-cell lung cancer: a phase I and pharmacokinetic study. Groen, H.J., van der Leest, A.H., de Vries, E.G., Uges, D.R., Szabó, B.G., Mulder, N.H. Br. J. Cancer (1995) [Pubmed]
  6. Chromosomal location and some structural features of human clathrin light-chain genes (CLTA and CLTB). Ponnambalam, S., Jackson, A.P., LeBeau, M.M., Pravtcheva, D., Ruddle, F.H., Alibert, C., Parham, P. Genomics (1994) [Pubmed]
  7. Clinical pharmacokinetics of carboplatin. Oguri, S., Sakakibara, T., Mase, H., Shimizu, T., Ishikawa, K., Kimura, K., Smyth, R.D. Journal of clinical pharmacology. (1988) [Pubmed]
  8. Regulation of the neuron-specific exon of clathrin light chain B. Stamm, S., Casper, D., Hanson, V., Helfman, D.M. Brain Res. Mol. Brain Res. (1999) [Pubmed]
  9. Plasma concentrations of 5-fluorouracil and its metabolites in colon cancer patients. Casale, F., Canaparo, R., Serpe, L., Muntoni, E., Pepa, C.D., Costa, M., Mairone, L., Zara, G.P., Fornari, G., Eandi, M. Pharmacol. Res. (2004) [Pubmed]
 
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