Centre for Brain Research, IISc
 

 

Faculty

Reddy P. Kommaddi's Lab

Home

Vivek Tiwari Profile:

Reddy P. Kommaddi

Senior Scientific Officer 

Research

Areas

G-protein coupled receptors.

Research Details

The G-protein coupled receptors are ubiquitously expressed and regulate most physiological processes. GPCRs function through β-arrestin adaptor proteins, which regulate receptor signal transduction and intracellular trafficking. β-arrestin2 ubiquitination promotes GPCR endocytosis and β-arrestin dependent signaling. Ubiquitination of β-arrestin2 and mGluRs may affect the abundance of synaptic proteins and neurotransmitter receptors at the synapse as well as morphological changes of synapse and spines in Alzheimer’s disease.
 We are trying to understand how ubiquitination and deubiquitination of mGluRs and β-arrestin2 contribute to the agonist induced synaptic functions in cellular models and mouse models of Alzheimer’s disease.
 Our research will provide new insights involving β-arrestin2 and mGluRs ubiquitination for therapeutic intervention and prevention of disease progression.

 

People

Position

Publications

  • Ahmad F, Das D, Kommaddi RP, Diwakar L, Gowaikar R, Rupanagudi KV, Bennett DA, Ravindranath V, (2018), Isoform-specific hyperactivation of calpain-2 occurs presymptomatically at the synapse in Alzheimer’s disease mice and correlates with memory deficits in human subjects, Scientific Reports, 8:, 13119
  • Kommaddi RP, Das D, Karunakaran S, Nanguneri S, Bapat D, Ray A, Shaw E, Bennett DA, Nair D, Ravindranath V, (2018), Aβ mediates F-actin disassembly in dendritic spines leading to cognitive deficits in Alzheimer’s disease, J Neuroscience, 38, 1085–1099
  • Ahmad F, Singh K, Das D, Gowaikar R, Shaw E, Ramachandran A, Rupanagudi KV, Kommaddi RP, Bennett DA, Ravindranath V, (2017), Reactive Oxygen Species-Mediated Loss of Synaptic Akt1 Signaling Leads to Deficient Activity-Dependent Protein Translation Early in Alzheimer’s Disease, Antioxid Redox Signal, 27(16):1269-1280
  • Jean-Charles PY, Yu SM, Abraham D, Kommaddi RP, Mao L, Strachan RT, Zhang ZS, Bowles DE, Brian L, Stiber JA, Jones SN, Koch WJ, Rockman HA, Shenoy SK, (2017), Mdm2 regulates cardiac contractility by inhibiting GRK2-mediated desensitization of β-adrenergic receptor signaling, JCI Insight, 2(17);pii: 95998
  • Feger BJ, Thompson JW, Dubois LG, Kommaddi RP, Foster MW, Mishra R, Shenoy SK, Shibata Y, Kidane YH, Moseley MA, Carnell LS, Bowles DE., (2016), Microgravity induces proteomics changes involved in endoplasmic reticulum stress and mitochondrial protection, Sci. Rep., 6:34091
  • Kommaddi RP, Jean-Charles PY, Shenoy SK.,, (2015), Phosphorylation of the deubiquitinase USP20 by protein kinase A regulates post-endocytic trafficking of beta2 adrenergic receptors to autophagosomes during physiological stress, J Biol Chem, 290(14):8888-903
  • Kommaddi RP, Shenoy SK, (2013), Arrestins and protein ubiquitination. Prog Mol Biol Transl Sci, 118:175-204. Review. PubMed PMID: 23764054.
  • Han SO, Kommaddi RP, Shenoy SK, (2013), Distinct roles for beta-arrestin2 and arrestin-domain-containing proteins in beta2 adrenergic receptor trafficking, EMBO Rep, 14(2):164-71. PMID: 23208550
  • Kommaddi RP, Dickson KM, Barker PA, (2011), Stress-induced expression of the p75neurotrophin receptor is regulated by O-GlcNAcylation of the Sp1 transcription factor, J Neurochem, 116(3):396-405. PMID: 21105874
  • Kommaddi RP, Thomas R, Ceni C, Daigneault K, Barker PA, (2011), Trk-dependent ADAM17 activation facilitates neurotrophin survival signaling, FASEB J, 25(6):2061-70. PMID: 21411748
  • Ceni C, Kommaddi RP, Thomas R, Vereker E, Liu X, McPherson PS, Ritter B, Barker PA, (2010), The p75NTR intracellular domain generated by neurotrophin-induced receptor cleavage potentiates Trk signaling, J Cell Sci, 123(Pt13):2299-307. PMID: 20530577
  • Contact

    Centre for Brain Research
    SID (Innovation centre) complex
    Indian Institute of Science (IISc)
    Malleswaram 18th Cross
    Bangalore-560012
    Karnataka, INDIA.

    Email: reddy@iisc.ac.in
    Telephone: Office +91 80 2293 3432