RHOA

From Wikipedia, the free encyclopedia


Ras homolog gene family, member A
PDB rendering based on 1a2b.
Available structures: 1a2b, 1cc0, 1cxz, 1dpf, 1ftn, 1kmq, 1lb1, 1ow3, 1s1c, 1tx4, 1x86, 1xcg, 1z2c, 2gcn, 2gco, 2gcp
Identifiers
Symbol(s) RHOA; ARH12; ARHA; RHO12; RHOH12
External IDs OMIM: 165390 MGI1096342 HomoloGene1257
RNA expression pattern

More reference expression data

Orthologs
Human Mouse
Entrez 387 11848
Ensembl ENSG00000067560 ENSMUSG00000007815
Uniprot P61586 Q3TN61
Refseq NM_001664 (mRNA)
NP_001655 (protein)
NM_016802 (mRNA)
NP_058082 (protein)
Location Chr 3: 49.37 - 49.42 Mb Chr 9: 108.16 - 108.2 Mb
Pubmed search [1] [2]

Ras homolog gene family, member A (RhoA) is a small GTPase protein known to regulate the actin cytoskeleton in the formation of stress fibers. It is encoded by the gene RHOA.

It acts upon two known effector proteins: ROCK1 (Rho-associated, coiled-coil containing protein kinase 1) and DIAPH1 (diaphanous homolog 1 (Drosophila)).

RhoA is part of a larger family of related proteins known as the Ras superfamily; proteins involved in the regulation and timing of cell division.

Contents

[edit] RhoA Pathway

Molecules act on various receptors, such as NgR1, LINGO1, p75, TROY and other unknown receptors (eg. by CSPGs), which stimulates RhoA. RhoA activates ROCK (RhoA kinase) which stimulates LIM kinase, which then stimulates Cofilin, which effectively re-organises the Actin cytoskeleton of the cell1. In the case of neurons, activation of this pathway results in growth cone collapse,1,3 therefore inhibits the growth and repair of neural pathways and axons. Inhibition of this pathway by its various components usually results in some level of improved remyelination.[1][2][3][4]


[edit] Further reading

  • Ramakers GJ (2002). "Rho proteins, mental retardation and the cellular basis of cognition.". Trends Neurosci. 25 (4): 191–9. PMID 11998687. 
  • Chang ZF, Lee HH (2006). "RhoA signaling in phorbol ester-induced apoptosis.". J. Biomed. Sci. 13 (2): 173–80. doi:10.1007/s11373-005-9056-4. PMID 16496227. 

[edit] Notes

  1. ^ YIU, G. & ZHIGANG, H. (2006). Glial inhibition of CNS axon regeneration. Nature Reviews Neuroscience, 7, 617-627
  2. ^ BRADBURY, E.J., MCMAHON, S.B. (2006). Spinal cord repair strategies: why do they work? Nature Reviews Neuroscience, 7, 644-653
  3. ^ KARNEZIS, T., MANDEMAKERS, W., MCQUALTER, J.L., ZHENG, B., HO, P.P., JORDAN, K.A., MURRAY, B.M., BARRES, B., TESSIER-LAVINGE, M., BERNARD, C.C.A. (2004). The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination. Nature Neuroscience, 7, 736-744
  4. ^ REGMAN, B.S., KUNKEL-BAGDEN, E., SCHNELL, L., DAI, H.N., GAO, D., SCHWAB, M.E. (1995). Recovery from spinal cord injury mediated by antibodies to neurite growth inhibitors. Nature, 378, 498-501

[edit] External links

Languages