TY - JOUR
T1 - Correction to
T2 - Intra-arterial Stem Cell Therapy Diminishes Inflammasome Activation After Ischemic Stroke: a Possible Role of Acid Sensing Ion Channel 1a (Journal of Molecular Neuroscience, (2021), 71, 2, (419-426), 10.1007/s12031-019-01460-3)
AU - Vats, Kanchan
AU - Sarmah, Deepaneeta
AU - Datta, Aishika
AU - Saraf, Jackson
AU - Kaur, Harpreet
AU - Pravalika, Kanta
AU - Wanve, Madhuri
AU - Kalia, Kiran
AU - Borah, Anupom
AU - Dave, Kunjan R.
AU - Yavagal, Dileep R.
AU - Bhattacharya, Pallab
N1 - Publisher Copyright:
© 2020, Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2021/2
Y1 - 2021/2
N2 - It has come to our notice that there was an inadvertent misupload of Fig. 2 (c, d) in the loading control (GAPDH) for ASIC1a and NLRP1 blots. We would like to replace the same with the correct image. This change anyhow does not affect the conclusion of the study. However, the use of GAPDH as a loading control for stroke studies sometimes is debatable (Zhai et al. 2014; Kang et al. 2018). Hence, we repeated our experiments to check the expression of ASIC1a and NLRP1 at different time points following stroke, using beta actin as a loading control. We found that at 24 h post stroke, maximal and significant expression of both ASIC1a and NLRP1 was observed (Fig. 2 e, f). The expression at 48 and 72 h post stroke were not significantly different as compared to that of sham. The expression results obtained using beta actin as a loading control were concurrent with the previous results published with GAPDH as a loading control. (Figure presented.).
AB - It has come to our notice that there was an inadvertent misupload of Fig. 2 (c, d) in the loading control (GAPDH) for ASIC1a and NLRP1 blots. We would like to replace the same with the correct image. This change anyhow does not affect the conclusion of the study. However, the use of GAPDH as a loading control for stroke studies sometimes is debatable (Zhai et al. 2014; Kang et al. 2018). Hence, we repeated our experiments to check the expression of ASIC1a and NLRP1 at different time points following stroke, using beta actin as a loading control. We found that at 24 h post stroke, maximal and significant expression of both ASIC1a and NLRP1 was observed (Fig. 2 e, f). The expression at 48 and 72 h post stroke were not significantly different as compared to that of sham. The expression results obtained using beta actin as a loading control were concurrent with the previous results published with GAPDH as a loading control. (Figure presented.).
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U2 - 10.1007/s12031-020-01731-4
DO - 10.1007/s12031-020-01731-4
M3 - Comment/debate
C2 - 33386587
AN - SCOPUS:85098509361
VL - 71
SP - 427
EP - 429
JO - Molecular and Chemical Neuropathology
JF - Molecular and Chemical Neuropathology
SN - 0895-8696
IS - 2
ER -