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Open Access Highly Accessed Research article

Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment

Sandeep Singh*, Varsheish Raina, Pavithra Lakshminarsimhan Chavali, Taronish Dubash, Sreenath Kadreppa, Pradeep Parab and Samit Chattopadhyay*

BMC Molecular Biology 2012, 13:28  doi:10.1186/1471-2199-13-28

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Minor changes of text in Introduction section

Dr. Samit Chattopadhyay   (2013-01-14 10:27)  NCCS, Ganeshkhind,Pune 411007, Maharashtra, India email

MS: 2060232625635356
Research article

Title: Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment.

Sandeep Singh, Varshiesh Raina, Pavithra Lakshminarsimhan Chavali, Taronish Dubash, Sreenath, Kadreppa, Pradeep Parab and Samit Chattopadhyay, BMC Molecular Biology 2012, 13:28

Page 1: Background section (from line no. 6 to line 17) might be read as follows:

Glutamic acid decarboxylase is already known to be involved in synthesis of a neurotransmitter inhibitor, GABA or Gamma-Amino butyric acid [2, 3]. While its role in neuronal activities is known, it is also shown to be involved in beta islet cells specific autoimmune reaction [4, 51]. Till date many of the type-1 diabetic patients are reported to have anti-GAD antibodies in circulation [4]. It has also been shown that non obese diabetic (NOD) mice when injected with GAD, have delayed onset of disease. The study has contributed this due to early toleration of auto reactive T cells due to GAD injections [4, 51].

51. Jun HS, Khil LY, Yoon JW: Role of glutamic acid decarboxylase in the pathogenesis of type 1 diabetes. Cell Mol Life Sci. 2002, 59(11):1892-901.

Page 2: Background section (from line no. 2 to line 15) might be read as follows:

Involvement of GABA as a signaling molecule between brain and pancreatic cells. Since GAD enzymes convert glutamic acid to gamma-amino butyric acid (GABA), thus they become very important molecules for proper functioning of the pancreatic cells [16, 17, 52]. Studies have shown the GAD expression is involved in autoimmune response leading to onset of the disease. One study in particular, showed that NOD mice, which were incorporated with antisense GAD, showed remarkably reduced onset of diabetes [18, 52]. Thus while GAD is critical for pancreatic function, but deregulation of GAD expression might be triggering disease onset.

Minor Change in the Reference:

52. Cara N: Glutamic Acid Decarboxylase and its role in the onset of Insulin-Dependent Diabetes Mellitus. Stanislaus Journal of Biochemical Reviews; May 2000.

Competing interests

None declared


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