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Disease relevance of Hindlimb

  • In rabbits with hindlimb ischemia, circulating EPCs were further augmented after pretreatment with GM-CSF, with a corresponding improvement in hindlimb neovascularization [1].
  • The amount of thrombin-antithrombin complex generated within the hindlimb preparation after pretreatment of the vasculature with purified Flavobacterium heparinase or with addition of platelet Factor IV to the hemostatic components, was equal to the uncatalyzed levels [2].
  • Targeted deletion of the Sp8 gene gives a striking phenotype, with severe truncation of both forelimbs and hindlimbs, absent tail, as well as defects in anterior and posterior neuropore closure leading to exencephaly and spina bifida [3].
  • Stimulation of endogenous nitric oxide pathway by L-arginine reduces declamp mortality and attenuates hypertension associated with aortic cross-clamp-induced hindlimb ischemia in rats [4].
  • The GAP-43 was elevated to statistically significant levels in forelimb, hindlimb, and parietal neocortical regions ipsilateral to the infarction only at days 3, 7, and 14 [5].

Psychiatry related information on Hindlimb

  • RESULTS: These mice display behavioral abnormalities similar to RTT phenotypes, including hindlimb clasping, impaired motor coordination, increased anxiety, and abnormal social behavior with other mice [6].
  • Maximal seizures were induced with electroshock via corneal electrodes, and phenytoin anticonvulsant effects were determined by measuring the duration of tonic hindlimb extension (THE) and prevention of the THE [7].
  • Overnight food deprivation resulted in a net mobilization of phenylalanine from whole-body proteins (P < 0.01) but not hindlimb proteins [8].
  • In acute low spinal and curarized preparations, the amplitude of the "spontaneous" fictive locomotor activities recorded from hindlimb muscle nerves after nialamide-DOPA pretreatment was much decreased in flexor and extensor nerves after MK-801 administration (0.25 mg/kg i.v.) whereas the locomotor period increased slightly [9].
  • The analgesic activity of O-(4-methoxylphenylcarbamoyl)-3-diethylaminopropiophenone oxime hydrochloride was investigated in Swiss--Webster mice using an electroshock technique in which the pain threshold was the minimum voltage producing tonic extension of the hindlimbs in response to an electroshock delivered to the feet [10].

High impact information on Hindlimb

  • Mice that are homozygous with respect to a mutation (ax(J)) in the ataxia (ax) gene develop severe tremors by 2-3 weeks of age followed by hindlimb paralysis and death by 6-10 weeks of age [11].
  • Homozygous mutant mice carrying a targeted deletion of Gdf11 exhibit anteriorly directed homeotic transformations throughout the axial skeleton and posterior displacement of the hindlimbs [12].
  • Herein we demonstrate that Osp null mice exhibit both neurological and reproductive deficits: CNS nerve conduction is slowed, hindlimb weakness is conspicuous, and males are sterile [13].
  • The genes Pitx1 and Tbx4 encode transcription factors that are expressed throughout the developing hindlimb but not forelimb buds [14].
  • Role of Pitx1 upstream of Tbx4 in specification of hindlimb identity [14].

Chemical compound and disease context of Hindlimb

  • We first administered L-arginine, previously shown to augment endogenous production of NO, to normal rabbits with operatively induced hindlimb ischemia [15].
  • We first analyzed the effect of diabetes (streptozotocin, 40 mg/kg) on BM-MNC pro-angiogenic potential in a model of surgically induced hindlimb ischemia [16].
  • Rats bearing rodent fibrosarcoma on the hindlimb underwent isolated limb infusion with saline, saline plus heat, l-phenylalanine mustard, l-phenylalanine mustard under conditions of normothermia, or l-phenylalanine mustard plus hyperthermia [17].
  • One mRNA that was more abundant in neck than in hindlimb muscles encoded the mouse ortholog of human AL-1 and chick RAGS, membrane-associated ligands of Eph tyrosine kinases that have recently been implicated in cortical axon fasciculation and retinotectal connectivity, respectively [18].
  • CONCLUSION: These results suggest that the recruitment of collateral vessels after the induction of hindlimb ischemia is significantly impaired in obese fa/fa Zucker rats due to a persistent vasoconstriction mediated by 5-HT and involving stimulation of 5-HT(1B) and/or 5-HT(2A) receptors [19].

Biological context of Hindlimb


Anatomical context of Hindlimb

  • Hox-5.2 antigen is detected strongly in developing fore- and hindlimb buds, where it forms a gradient of nuclear protein throughout most of the mesenchyme [25].
  • Pitx1 is a Bicoid-related homeodomain factor that exhibits preferential expression in the hindlimb, as well as expression in the developing anterior pituitary gland and first branchial arch [21].
  • Mice homozygous for the mutation exhibit tremors and contraction of hindlimbs. betaIV-spectrin expression is mostly restricted to neurons, where it colocalizes with and binds to ankyrin-G at axon initial segments (AISs) and nodes of Ranvier (NR) [26].
  • These results indicate that glycinergic neurons in or near the anterior hindlimb enlargement contribute to the overall timing of the rostral scratch rhythm and to the recruitment timing of individual hip flexor motor neurons within each scratch burst [27].
  • We show that, together, Pitx1 and Pitx2 are required for formation of hindlimb buds and, when present in limited doses, for development of proximal (femur) and anterior (tibia and digit 1) hindlimb structures [28].

Associations of Hindlimb with chemical compounds


Gene context of Hindlimb

  • Among them are the loss of Hoxd10 function, the sum of remaining Hoxd gene activity, and the ectopic gain of function of the neighboring gene Evx2, all contributing to the mispositioning, the absence, or misidentification of specific lumbo-sacral pools of motoneurons, nerve root homeosis, and hindlimb innervation defects [34].
  • In the present study, mice with a knockout of the p105/p50 (Nfkb1) gene are shown to be resistant to the decrease in soleus fiber cross-sectional area that results from 10 days of hindlimb unloading [35].
  • To study the potential angiogenic capacity of BDNF in mediating the neovascularization of ischemic and non-ischemic adult mouse tissues, we utilized a hindlimb ischemia and a subcutaneous Matrigel model [36].
  • Pitx1 and Pitx2 are required for development of hindlimb buds [28].
  • Phenotypes of double and triple mutants reveal that Hoxb8, Hoxc8 and Hoxd8 have redundant functions at upper thoracic and sacral levels, including positioning of the hindlimbs [37].

Analytical, diagnostic and therapeutic context of Hindlimb


  1. Ischemia- and cytokine-induced mobilization of bone marrow-derived endothelial progenitor cells for neovascularization. Takahashi, T., Kalka, C., Masuda, H., Chen, D., Silver, M., Kearney, M., Magner, M., Isner, J.M., Asahara, T. Nat. Med. (1999) [Pubmed]
  2. Acceleration of thrombin-antithrombin complex formation in rat hindquarters via heparinlike molecules bound to the endothelium. Marcum, J.A., McKenney, J.B., Rosenberg, R.D. J. Clin. Invest. (1984) [Pubmed]
  3. Sp8 is crucial for limb outgrowth and neuropore closure. Bell, S.M., Schreiner, C.M., Waclaw, R.R., Campbell, K., Potter, S.S., Scott, W.J. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  4. Stimulation of endogenous nitric oxide pathway by L-arginine reduces declamp mortality and attenuates hypertension associated with aortic cross-clamp-induced hindlimb ischemia in rats. Jin, J.S., D'Alecy, L.G. Hypertension (1995) [Pubmed]
  5. Enhanced neocortical neural sprouting, synaptogenesis, and behavioral recovery with D-amphetamine therapy after neocortical infarction in rats. Stroemer, R.P., Kent, T.A., Hulsebosch, C.E. Stroke (1998) [Pubmed]
  6. Postnatal loss of methyl-CpG binding protein 2 in the forebrain is sufficient to mediate behavioral aspects of Rett syndrome in mice. Gemelli, T., Berton, O., Nelson, E.D., Perrotti, L.I., Jaenisch, R., Monteggia, L.M. Biol. Psychiatry (2006) [Pubmed]
  7. A comparative study of the effects of phenytoin and phenobarbital on electrically induced maximal seizures in frogs and mice. Johnson, S.W., Riker, W.K. J. Pharmacol. Exp. Ther. (1982) [Pubmed]
  8. Whole-body and hindlimb protein breakdown are differentially altered by feeding in neonatal piglets. Thivierge, M.C., Bush, J.A., Suryawan, A., Nguyen, H.V., Orellana, R.A., Burrin, D.G., Jahoor, F., Davis, T.A. J. Nutr. (2005) [Pubmed]
  9. Effects of an NMDA-receptor antagonist, MK-801, on central locomotor programming in the rabbit. Fenaux, F., Corio, M., Palisses, R., Viala, D. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (1991) [Pubmed]
  10. Comparative analgesic, behavioral, and dependence properties of morphine and O-(4-methoxylphenylcarbamoyl)-3-diethylaminopropiophenone oxime hydrochloride. Watzman, N., Buckley, J.P. Journal of pharmaceutical sciences. (1980) [Pubmed]
  11. Synaptic defects in ataxia mice result from a mutation in Usp14, encoding a ubiquitin-specific protease. Wilson, S.M., Bhattacharyya, B., Rachel, R.A., Coppola, V., Tessarollo, L., Householder, D.B., Fletcher, C.F., Miller, R.J., Copeland, N.G., Jenkins, N.A. Nat. Genet. (2002) [Pubmed]
  12. Regulation of anterior/posterior patterning of the axial skeleton by growth/differentiation factor 11. McPherron, A.C., Lawler, A.M., Lee, S.J. Nat. Genet. (1999) [Pubmed]
  13. CNS myelin and sertoli cell tight junction strands are absent in Osp/claudin-11 null mice. Gow, A., Southwood, C.M., Li, J.S., Pariali, M., Riordan, G.P., Brodie, S.E., Danias, J., Bronstein, J.M., Kachar, B., Lazzarini, R.A. Cell (1999) [Pubmed]
  14. Role of Pitx1 upstream of Tbx4 in specification of hindlimb identity. Logan, M., Tabin, C.J. Science (1999) [Pubmed]
  15. Nitric oxide synthase modulates angiogenesis in response to tissue ischemia. Murohara, T., Asahara, T., Silver, M., Bauters, C., Masuda, H., Kalka, C., Kearney, M., Chen, D., Symes, J.F., Fishman, M.C., Huang, P.L., Isner, J.M. J. Clin. Invest. (1998) [Pubmed]
  16. Impairment in ischemia-induced neovascularization in diabetes: bone marrow mononuclear cell dysfunction and therapeutic potential of placenta growth factor treatment. Tamarat, R., Silvestre, J.S., Le Ricousse-Roussanne, S., Barateau, V., Lecomte-Raclet, L., Clergue, M., Duriez, M., Tobelem, G., Lévy, B.I. Am. J. Pathol. (2004) [Pubmed]
  17. The role of hyperthermia in regional alkylating agent chemotherapy. Abdel-Wahab, O.I., Grubbs, E., Viglianti, B.L., Cheng, T.Y., Ueno, T., Ko, S., Rabbani, Z., Curtis, S., Pruitt, S.K., Dewhirst, M.W., Tyler, D.S. Clin. Cancer Res. (2004) [Pubmed]
  18. The Eph kinase ligand AL-1 is expressed by rostral muscles and inhibits outgrowth from caudal neurons. Donoghue, M.J., Lewis, R.M., Merlie, J.P., Sanes, J.R. Mol. Cell. Neurosci. (1996) [Pubmed]
  19. Serotonin receptor blockade improves distal perfusion after lower limb ischemia in the fatty Zucker rat. Janiak, P., Lainée, P., Grataloup, Y., Luyt, C.E., Bidouard, J.P., Michel, J.B., O'Connor, S.E., Herbert, J.M. Cardiovasc. Res. (2002) [Pubmed]
  20. Divergent functions of murine Pax3 and Pax7 in limb muscle development. Relaix, F., Rocancourt, D., Mansouri, A., Buckingham, M. Genes Dev. (2004) [Pubmed]
  21. Role of the Bicoid-related homeodomain factor Pitx1 in specifying hindlimb morphogenesis and pituitary development. Szeto, D.P., Rodriguez-Esteban, C., Ryan, A.K., O'Connell, S.M., Liu, F., Kioussi, C., Gleiberman, A.S., Izpisúa-Belmonte, J.C., Rosenfeld, M.G. Genes Dev. (1999) [Pubmed]
  22. Physiologic characterization of endothelin A and B receptor activity in the ovine fetal pulmonary circulation. Ivy, D.D., Kinsella, J.P., Abman, S.H. J. Clin. Invest. (1994) [Pubmed]
  23. ATP-sensitive potassium channels mediate contraction-induced attenuation of sympathetic vasoconstriction in rat skeletal muscle. Thomas, G.D., Hansen, J., Victor, R.G. J. Clin. Invest. (1997) [Pubmed]
  24. Stable gene transfer and expression of human blood coagulation factor IX after intramuscular injection of recombinant adeno-associated virus. Herzog, R.W., Hagstrom, J.N., Kung, S.H., Tai, S.J., Wilson, J.M., Fisher, K.J., High, K.A. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  25. Complementary homeo protein gradients in developing limb buds. Oliver, G., Sidell, N., Fiske, W., Heinzmann, C., Mohandas, T., Sparkes, R.S., De Robertis, E.M. Genes Dev. (1989) [Pubmed]
  26. [Beta]IV-spectrin regulates sodium channel clustering through ankyrin-G at axon initial segments and nodes of Ranvier. Komada, M., Soriano, P. J. Cell Biol. (2002) [Pubmed]
  27. Glycinergic inhibition contributes to the generation of rostral scratch motor patterns in the turtle spinal cord. Currie, S.N., Lee, S. J. Neurosci. (1997) [Pubmed]
  28. Pitx1 and Pitx2 are required for development of hindlimb buds. Marcil, A., Dumontier, E., Chamberland, M., Camper, S.A., Drouin, J. Development (2003) [Pubmed]
  29. Pax9-deficient mice lack pharyngeal pouch derivatives and teeth and exhibit craniofacial and limb abnormalities. Peters, H., Neubüser, A., Kratochwil, K., Balling, R. Genes Dev. (1998) [Pubmed]
  30. Effect of denervation on the expression of two glucose transporter isoforms in rat hindlimb muscle. Block, N.E., Menick, D.R., Robinson, K.A., Buse, M.G. J. Clin. Invest. (1991) [Pubmed]
  31. Diabetes-induced functional and structural changes in insulin receptors from rat skeletal muscle. Burant, C.F., Treutelaar, M.K., Buse, M.G. J. Clin. Invest. (1986) [Pubmed]
  32. Effects of dietary L-arginine on atherosclerosis and endothelium-dependent vasodilatation in the hypercholesterolemic rabbit. Response according to treatment duration, anatomic site, and sex. Jeremy, R.W., McCarron, H., Sullivan, D. Circulation (1996) [Pubmed]
  33. An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice. Brandes, R.P., Schmitz-Winnenthal, F.H., Félétou, M., Gödecke, A., Huang, P.L., Vanhoutte, P.M., Fleming, I., Busse, R. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  34. HoxD cluster scanning deletions identify multiple defects leading to paralysis in the mouse mutant Ironside. Tarchini, B., Huynh, T.H., Cox, G.A., Duboule, D. Genes Dev. (2005) [Pubmed]
  35. Disruption of either the Nfkb1 or the Bcl3 gene inhibits skeletal muscle atrophy. Hunter, R.B., Kandarian, S.C. J. Clin. Invest. (2004) [Pubmed]
  36. Neurotrophins promote revascularization by local recruitment of TrkB+ endothelial cells and systemic mobilization of hematopoietic progenitors. Kermani, P., Rafii, D., Jin, D.K., Whitlock, P., Schaffer, W., Chiang, A., Vincent, L., Friedrich, M., Shido, K., Hackett, N.R., Crystal, R.G., Rafii, S., Hempstead, B.L. J. Clin. Invest. (2005) [Pubmed]
  37. Axial skeletal patterning in mice lacking all paralogous group 8 Hox genes. van den Akker, E., Fromental-Ramain, C., de Graaff, W., Le Mouellic, H., Brûlet, P., Chambon, P., Deschamps, J. Development (2001) [Pubmed]
  38. Neuropeptide Y induces ischemic angiogenesis and restores function of ischemic skeletal muscles. Lee, E.W., Michalkiewicz, M., Kitlinska, J., Kalezic, I., Switalska, H., Yoo, P., Sangkharat, A., Ji, H., Li, L., Michalkiewicz, T., Ljubisavljevic, M., Johansson, H., Grant, D.S., Zukowska, Z. J. Clin. Invest. (2003) [Pubmed]
  39. Hypotensive action of parathyroid hormone preparations on rats and dogs. Pang, P.K., Tenner, T.E., Yee, J.A., Yang, M., Janssen, H.F. Proc. Natl. Acad. Sci. U.S.A. (1980) [Pubmed]
  40. The effects of intrathecal administration of excitatory amino acid agonists and antagonists on the initiation of locomotion in the adult cat. Douglas, J.R., Noga, B.R., Dai, X., Jordan, L.M. J. Neurosci. (1993) [Pubmed]
  41. Spinalization unmasks clonidine's alpha 1-adrenergic mediated excitation of the flexor reflex in rats. Kehne, J.H., Gallager, D.W., Davis, M. J. Neurosci. (1985) [Pubmed]
  42. Sarcolemmal damage in dystrophin deficiency is modulated by synergistic interactions between mechanical and oxidative/nitrosative stresses. Dudley, R.W., Danialou, G., Govindaraju, K., Lands, L., Eidelman, D.E., Petrof, B.J. Am. J. Pathol. (2006) [Pubmed]
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