Kanaga SABAPATHY  
                       
    Main Page   Publications              
                       
   
filler filler filler
  Recent Publications  
 

“Distinct roles for JNK1 and JNK2 in regulating JNK activity and c-Jun-dependent cell proliferation”.
Sabapathy K*, Hochedlinger K, Nam SY, Bauer A, Karin M, Wagner EF.
Molecular Cell.  2004.15(5):713-25.

“JNK2 – A negative regulator of cellular proliferation”.
Sabapathy K, Wagner EF.
Cell Cycle. 2004. 3(12):1520-3.

“Multiple stress signals induce p73b accumulation”. 
Lin KW, Nam SY, Toh WH, Dulloo I, Sabapathy K. 
Neoplasia. 2004. 6(5): 546-57.

“c-Jun regulates the stability and activity of the p53 homologue, p73”. 
Toh WH, Siddique MM, Boominathan L, Lin KW, Sabapathy K.
J Biol Chem. 2004.  279(43):44713-22.

“Ectopic mTERT expression in mouse embryonic stem cells does not affect differentiation but confers resistance to differentiation- and stress-induced p53-dependent apoptosis”. 
Lee MK, Hande MP, Sabapathy K.
J Cell Science. 2005. 118(4):819-29.

“Impaired long-term potentiation in c-Jun N-terminal kinase 2 deficient mice”. 
Chen JT, Lu DH, Chia CP, Ruan DY, Sabapathy K*, Xiao ZC*. 
J. Neurochem. 2005. 93(2):463-73.  *: co-corresponding senior authors

“Relief of p53-mediated telomerase suppression by p73”.
Toh WH, Kyo S, Sabapathy K.
J Biol Chem. 2005. 280(17):17329-38.

“Evaluation of the combined effect of p53 codon 72 polymorphism and hot-spot mutations in response to anticancer drugs”. 
Vikhanskaya F, Siddique MM, Broggini M, Sabapathy K.
Clin Cancer Research. 2005. 11:4348-56.

“Transactivation-dependent and independent regulation of p73 stability”. 
Dulloo I, Sabapathy K.
J Biol Chem. 2005. 280:28203-14.

“Evidence for selective expression of the p53 codon 72 polymorphs: implications in cancer development”. 
Siddique MM, Balram C, Fiszer-Maliszewska L, Aggarwal A, Tan A, Tan P, Soo KC, Sabapathy K.
Cancer, Epidem., Biomarkers & Prevention. 2005. 14:2245-52.

“Trp53-dependent DNA-repair is affected by the codon 72 polymorphism”.
Siddique MM, Sabapathy K.
Oncogene. 2006. 5:3489-500. 

“Aflatoxin-B1 exposure does not lead to p53 mutations but results in enhanced hepatocellular carcinoma formation in Hupki (human p53 knock in) mice”.
Tong WM, Lee MK, Galendo D, Wang ZQ, Sabapathy K.
Int J Cancer. 2006.119:745-9.

“c-Jun promotes cellular survival by suppression of PTEN“.
Hettinger K, Vikhanskaya F, Poh MK, Lee MK, de Belle I, Zhang JT, Reddy SAG,  Sabapathy K.
Cell Death & Diffen. 2007.14:218-29.

“JNK1 contributes to metabotropic glutamate receptor-dependent long-term depression and short-term synaptic plasticity in the mice area hippocampal CA1”.
Li XM, Li CC, Yu SS, Chen JT, Sabapathy K*, Ruan DY*.
Eur J Neurosci. 2007. 25:391-6. *: co-corresponding author

“The codon 72 polymorphism-specific effects of human p53 are absent in mouse cells – implications on generation of mouse models”. 
Phang BH, Sabapathy K. 
Oncogene. 2007. 26:2964-74.

“Cancer-derived p53 mutants suppress p53-dependent target gene expression –potential mechanism for gain of function of mutant p53”. 
Vikhansyaka F, Lee MK, Mazzoletti M, Broggini M, Sabapathy K.
Nucleic Acid Research. 2007. 35:2093-104.

“p73 supports cellular growth through c-Jun-dependent AP-1 transactivation”. 
Vikhansyaka F, Toh WH, Dulloo I, Wu Q, Boominathan L, Ng HH, Vousden K, Sabapathy K.
Nature Cell Biol. 2007.9:698-705.

“Phosphorylation at the carboxyl terminal S373 and S375 residues and 14-3-3 binding are not required for mouse p53 function”. 
Lee MK, Sabapathy K.
Neoplasia. 2007. 9:690-8.

“The tumor-suppressor p53 is not required for pancreatic beta cell death during diabetes and upon irradiation”.
Nam SY, Lee MK, Sabapathy K.
J Physiol (London). 2008. 586:407-17.

“MDM2 SNP309 G allele decreases risk but does not affect onset-age or survival of Chinese leukaemia patients”. 
Phang BH, Linn YC, Li H, Sabapathy K.
Eur J Cancer. 2008. 44:760-6.

“MDM2 SNP309 G allele increases risk but the T allele is associated with earlier onset-age of sporadic breast cancers in the Chinese population”. 
Lum SS, Chua HW, Li H, Li WF, Rao N, Wei J, Shao Z, Sabapathy K. 
Carcinogenesis.  2008. 29:754-61.

“The R246S hot-spot p53 mutant exerts dominant-negative effects in embryonic stem cells in vitro and in vivo”. 
Lee MK, Sabapathy K. 
J Cell Science. 2008. 21:1899-906.

“Defective MHC class I antigen surface expression promotes cellular survival through elevated ER stress and modulation of p53 function”. 
Sabapathy K, Nam SY.  |
Cell Death & Diffen. 2008.15:1364-74.

“TAp73b and DNp73b activate the expression of the pro-survival caspase-2S”.
Toh WH, Logette E, Corcos L, Sabapathy K. 
Nucleic Acids Res. 2008. 36:4498-509.

“Tyrosine 170 is dispensable for c-Jun turnover”. 
Xie M, Sabapathy K. 
Cell Signal.   2010. 22:330-7.

“An essential role for p73 in regulating mitotic cell death”.
Toh WH, Nam SY, Sabapathy K. 
Cell Death & Diffen. 2010. 17:787-800.

“The anti-apoptotic DeltaNp73 is degraded in a c-Jun-dependent manner upon genotoxic stress through the antizyme-mediated pathway”. 
Dulloo I, Gopalan G, Melino G, Sabapathy K. 
Proc Nat Acad Sci. 2010. 107:4902-7. 

“Effect of MDM2 SNP309 and p53 codon 72 polymorphisms on lung cancer risk and survival among non-smoking Chinese women in Singapore”. 
Chua HW, Ng D, Choo S, Lum SS, Li H, Soh LY, Sabapathy K*, Seow A*. 
BMC Cancer. 2010. 10:88.   *: co-corresponding author

“Serine 312 phosphorylation is dispensable for wild-type p53 functions in vivo”.  Lee MK, Tong WN, Wang ZQ, Sabapathy K. 
Cell Death & Diffn. 2011. 18:214-21.

“Characterization of novel and uncharacterized p53 SNPs in the Chinese population –intron 2 SNP co-segregates with the common codon 72 polymorphism”. 
Phang BH, Chua HW, Li HH, Linn YC, Sabapathy K. 
PLOSOne.  2011. 6(1):e15320.

“p53 promotes cellular survival in a context dependent manner by directly inducing the expression of heme-oxygenase-1”. 
Nam SY, Sabapathy K. 
Oncogene. 2011. 30(44):4476-86.

“JNK1 and JNK2 play redundant functions in Myc-induced B cell lymphoma formation.” 
Anbalagan M, Sabapathy K. 
Int J Cancer. 2012. 130(8):1967-9.

“Cell-type, dose and mutation-type specificity dictate mutant p53 functions in vivo.” 
Lee MK, Teoh WW, Phang BH, Tong WM, Wang ZQ and Sabapathy K.
Cancer Cell. 2012. 22(6):751-64.

“Role of JNKs in human diseases“. 
Sabapathy K. 
In Protein Phosphorylation in Health and Disease.
Edited by Shirish Shenolikar. 106, PMBTS, UK: Academic Press. 106:145-69.  2012.

“The C(ancer) and D(evelopmental) roles of p63 and p73.” 
Sabapathy K, Nagakawara A, Aberdam D. 
Cell Death Differ. 2014. 21(8):1340-2.

“Suppression of acetylpolyamine oxidase by selected AP-1 members regulate DNp73 abundance – mechanistic insights for overcoming DNp73-mediated resistance to chemotherapeutic drugs.”
Bunjobpol W, Dulloo I, Igarashi K, Concin N, Matsuo K and Sabapathy K. 
Cell Death Differ. 2014. 21(8):1240-9.

“Hypoxia-inducible TAp73 regulates the angiogenic transcriptome and supports tumorigenesis.”
Dulloo I, Phang BH, Othman R, Tan SY, Vijayaraghavan A, Goh LK, Martin-Lopez M, Marques MM, Li CW, Wang DY, Marin MC, Xian W, McKeon F and Sabapathy K. 
Nature Cell Biol.  2015.  17(4):511-23.

“Molecular characterization of hepatocarcinogenesis using mouse models.” 
Teoh WW, Xie M, Vijayaraghavan A, Yaligar J, Tong WM, Goh LK and Sabapathy K. 
Disease Models and Mechanisms. 2015. 
Dis Model Mech. 2015. 8(7):743-53.

“Interplay between TAp73 and selected Activator Protein-1 family members promotes AP-1 target gene activation and cellular growth”. 
Subramanian D, Bunjobpol W, Sabapathy K. 
J Biol Chem. 2015 May 27. pii: jbc.M115.636548. [Epub ahead of print].

 


 

 
filler filler filler