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Correction for Gabai et al., "Heat Shock Transcription Factor Hsf1 Is Involved in Tumor Progression via Regulation of Hypoxia-Inducible Factor 1 and RNA-Binding Protein HuR".

Molecular and cellular biology

Gabai VL, Meng L, Kim G, Mills TA, Benjamin IJ, Sherman MY.
PMID: 28951485
Mol Cell Biol. 2017 Sep 26;37(20). doi: 10.1128/MCB.00415-17. Print 2017 Oct 15.

No abstract available.

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Gabai VL, Meng L, Kim G, et al. Correction for Gabai et al., "Heat Shock Transcription Factor Hsf1 Is Involved in Tumor Progression via Regulation of Hypoxia-Inducible Factor 1 and RNA-Binding Protein HuR". Mol Cell Biol. 2017;37(20)doi: 10.1128/MCB.00415-17.
Gabai, V. L., Meng, L., Kim, G., Mills, T. A., Benjamin, I. J., & Sherman, M. Y. (2017). Correction for Gabai et al., "Heat Shock Transcription Factor Hsf1 Is Involved in Tumor Progression via Regulation of Hypoxia-Inducible Factor 1 and RNA-Binding Protein HuR". Molecular and cellular biology, 37(20), . https://doi.org/10.1128/MCB.00415-17
Gabai, Vladimir L, et al. "Correction for Gabai et al., "Heat Shock Transcription Factor Hsf1 Is Involved in Tumor Progression via Regulation of Hypoxia-Inducible Factor 1 and RNA-Binding Protein HuR"." Molecular and cellular biology vol. 37,20 (2017). doi: https://doi.org/10.1128/MCB.00415-17
Gabai VL, Meng L, Kim G, Mills TA, Benjamin IJ, Sherman MY. Correction for Gabai et al., "Heat Shock Transcription Factor Hsf1 Is Involved in Tumor Progression via Regulation of Hypoxia-Inducible Factor 1 and RNA-Binding Protein HuR". Mol Cell Biol. 2017 Sep 26;37(20). doi: 10.1128/MCB.00415-17. Print 2017 Oct 15. PMID: 28951485; PMCID: PMC5615190.
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Mechanisms and in vivo functions of contact inhibition of locomotion.

Nature reviews. Molecular cell biology

Stramer B, Mayor R.
PMID: 27677859
Nat Rev Mol Cell Biol. 2017 Jan;18(1):43-55. doi: 10.1038/nrm.2016.118. Epub 2016 Sep 28.

Contact inhibition of locomotion (CIL) is a process whereby a cell ceases motility or changes its trajectory upon collision with another cell. CIL was initially characterized more than half a century ago and became a widely studied model system...

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Stramer B, Mayor R. Mechanisms and in vivo functions of contact inhibition of locomotion. Nat Rev Mol Cell Biol. 2016;18(1):43-55doi: 10.1038/nrm.2016.118.
Stramer, B., & Mayor, R. (2017). Mechanisms and in vivo functions of contact inhibition of locomotion. Nature reviews. Molecular cell biology, 18(1), 43-55. https://doi.org/10.1038/nrm.2016.118
Stramer, Brian, and Mayor, Roberto. "Mechanisms and in vivo functions of contact inhibition of locomotion." Nature reviews. Molecular cell biology vol. 18,1 (2017): 43-55. doi: https://doi.org/10.1038/nrm.2016.118
Stramer B, Mayor R. Mechanisms and in vivo functions of contact inhibition of locomotion. Nat Rev Mol Cell Biol. 2017 Jan;18(1):43-55. doi: 10.1038/nrm.2016.118. Epub 2016 Sep 28. PMID: 27677859.
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TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis.

Molecular cell

Pan JA, Sun Y, Jiang YP, Bott AJ, Jaber N, Dou Z, Yang B, Chen JS, Catanzaro JM, Du C, Ding WX, Diaz-Meco MT, Moscat J, Ozato K, Lin RZ, Zong WX.
PMID: 27058791
Mol Cell. 2016 Apr 07;62(1):149-51. doi: 10.1016/j.molcel.2016.03.015.

No abstract available.

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Pan JA, Sun Y, Jiang YP, et al. TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis. Mol Cell. 2016;62(1):149-51doi: 10.1016/j.molcel.2016.03.015.
Pan, J. A., Sun, Y., Jiang, Y. P., Bott, A. J., Jaber, N., Dou, Z., Yang, B., Chen, J. S., Catanzaro, J. M., Du, C., Ding, W. X., Diaz-Meco, M. T., Moscat, J., Ozato, K., Lin, R. Z., & Zong, W. X. (2016). TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis. Molecular cell, 62(1), 149-51. https://doi.org/10.1016/j.molcel.2016.03.015
Pan, Ji-An, et al. "TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis." Molecular cell vol. 62,1 (2016): 149-51. doi: https://doi.org/10.1016/j.molcel.2016.03.015
Pan JA, Sun Y, Jiang YP, Bott AJ, Jaber N, Dou Z, Yang B, Chen JS, Catanzaro JM, Du C, Ding WX, Diaz-Meco MT, Moscat J, Ozato K, Lin RZ, Zong WX. TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis. Mol Cell. 2016 Apr 07;62(1):149-51. doi: 10.1016/j.molcel.2016.03.015. PMID: 27058791.
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Isolation and Characterization of Actinobacteria from Algerian Sahara Soils with Antimicrobial Activities.

International journal of molecular and cellular medicine

Mohamed H, Miloud B, Zohra F, García-Arenzana JM, Veloso A, Rodríguez-Couto S.
PMID: 28890887
Int J Mol Cell Med. 2017;6(2):109-120. doi: 10.22088/acadpub.BUMS.6.2.5. Epub 2017 Jul 11.

Extreme ecosystems can be a source of untapped microorganisms to produce novel bioactive compounds of industrial interest. Consequently, in this work, 32 actinomycetes were isolated from 6 soil samples collected from Algerian Sahara in searching for untapped producers of...

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Mohamed H, Miloud B, Zohra F, et al. Isolation and Characterization of Actinobacteria from Algerian Sahara Soils with Antimicrobial Activities. Int J Mol Cell Med. 2017;6(2):109-120doi: 10.22088/acadpub.BUMS.6.2.5.
Mohamed, H., Miloud, B., Zohra, F., García-Arenzana, J. M., Veloso, A., & Rodríguez-Couto, S. (2017). Isolation and Characterization of Actinobacteria from Algerian Sahara Soils with Antimicrobial Activities. International journal of molecular and cellular medicine, 6(2), 109-120. https://doi.org/10.22088/acadpub.BUMS.6.2.5
Mohamed, Harir, et al. "Isolation and Characterization of Actinobacteria from Algerian Sahara Soils with Antimicrobial Activities." International journal of molecular and cellular medicine vol. 6,2 (2017): 109-120. doi: https://doi.org/10.22088/acadpub.BUMS.6.2.5
Mohamed H, Miloud B, Zohra F, García-Arenzana JM, Veloso A, Rodríguez-Couto S. Isolation and Characterization of Actinobacteria from Algerian Sahara Soils with Antimicrobial Activities. Int J Mol Cell Med. 2017;6(2):109-120. doi: 10.22088/acadpub.BUMS.6.2.5. Epub 2017 Jul 11. PMID: 28890887; PMCID: PMC5581552.
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Correction for Pedersen et al., Regulation of CARD11 Signaling and Lymphoma Cell Survival by the E3 Ubiquitin Ligase RNF181.

Molecular and cellular biology

Pedersen SM, Chan W, Jattani RP, Mackie dS, Pomerantz JL.
PMID: 27034408
Mol Cell Biol. 2016 Mar 31;36(8):1322. doi: 10.1128/MCB.00106-16. Print 2016 Apr.

No abstract available.

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Pedersen SM, Chan W, Jattani RP, et al. Correction for Pedersen et al., Regulation of CARD11 Signaling and Lymphoma Cell Survival by the E3 Ubiquitin Ligase RNF181. Mol Cell Biol. 2016;36(8):1322doi: 10.1128/MCB.00106-16.
Pedersen, S. M., Chan, W., Jattani, R. P., Mackie, d. S., & Pomerantz, J. L. (2016). Correction for Pedersen et al., Regulation of CARD11 Signaling and Lymphoma Cell Survival by the E3 Ubiquitin Ligase RNF181. Molecular and cellular biology, 36(8), 1322. https://doi.org/10.1128/MCB.00106-16
Pedersen, Sarah M, et al. "Correction for Pedersen et al., Regulation of CARD11 Signaling and Lymphoma Cell Survival by the E3 Ubiquitin Ligase RNF181." Molecular and cellular biology vol. 36,8 (2016): 1322. doi: https://doi.org/10.1128/MCB.00106-16
Pedersen SM, Chan W, Jattani RP, Mackie dS, Pomerantz JL. Correction for Pedersen et al., Regulation of CARD11 Signaling and Lymphoma Cell Survival by the E3 Ubiquitin Ligase RNF181. Mol Cell Biol. 2016 Mar 31;36(8):1322. doi: 10.1128/MCB.00106-16. Print 2016 Apr. PMID: 27034408; PMCID: PMC4836273.
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Metabolic stressors disrupt proteome homeostasis to suppress malignancy.

Molecular & cellular oncology

Dai C.
PMID: 26973866
Mol Cell Oncol. 2015;2(4). doi: 10.1080/23723556.2014.1002718. Epub 2015 Jan 23.

Within tumor cells the heat shock factor 1 (HSF1)-mediated stress response is constitutively mobilized to counter persistent proteotoxic stress, hence sustaining their fragile proteome homeostasis and supporting robust malignant phenotypes. Intriguingly, our new studies reveal that metabolic stressors, such...

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Dai C. Metabolic stressors disrupt proteome homeostasis to suppress malignancy. Mol Cell Oncol. 2015;2(4)doi: 10.1080/23723556.2014.1002718.
Dai, C. (2015). Metabolic stressors disrupt proteome homeostasis to suppress malignancy. Molecular & cellular oncology, 2(4), . https://doi.org/10.1080/23723556.2014.1002718
Dai, Chengkai. "Metabolic stressors disrupt proteome homeostasis to suppress malignancy." Molecular & cellular oncology vol. 2,4 (2015). doi: https://doi.org/10.1080/23723556.2014.1002718
Dai C. Metabolic stressors disrupt proteome homeostasis to suppress malignancy. Mol Cell Oncol. 2015;2(4). doi: 10.1080/23723556.2014.1002718. Epub 2015 Jan 23. PMID: 26973866; PMCID: PMC4786015.
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Correction for Yin and Smolikove, Impaired Resection of Meiotic Double-Strand Breaks Channels Repair to Nonhomologous End Joining in Caenorhabditis elegans.

Molecular and cellular biology

Yin Y, Smolikove S.
PMID: 26093000
Mol Cell Biol. 2015 Jul;35(14):2568. doi: 10.1128/MCB.00504-15.

No abstract available.

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Yin Y, Smolikove S. Correction for Yin and Smolikove, Impaired Resection of Meiotic Double-Strand Breaks Channels Repair to Nonhomologous End Joining in Caenorhabditis elegans. Mol Cell Biol. 2015;35(14):2568doi: 10.1128/MCB.00504-15.
Yin, Y., & Smolikove, S. (2015). Correction for Yin and Smolikove, Impaired Resection of Meiotic Double-Strand Breaks Channels Repair to Nonhomologous End Joining in Caenorhabditis elegans. Molecular and cellular biology, 35(14), 2568. https://doi.org/10.1128/MCB.00504-15
Yin, Yizhi, and Smolikove, Sarit. "Correction for Yin and Smolikove, Impaired Resection of Meiotic Double-Strand Breaks Channels Repair to Nonhomologous End Joining in Caenorhabditis elegans." Molecular and cellular biology vol. 35,14 (2015): 2568. doi: https://doi.org/10.1128/MCB.00504-15
Yin Y, Smolikove S. Correction for Yin and Smolikove, Impaired Resection of Meiotic Double-Strand Breaks Channels Repair to Nonhomologous End Joining in Caenorhabditis elegans. Mol Cell Biol. 2015 Jul;35(14):2568. doi: 10.1128/MCB.00504-15. PMID: 26093000; PMCID: PMC4475918.
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Rab11 in disease progression.

International journal of molecular and cellular medicine

Bhuin T, Roy JK.
PMID: 25815277
Int J Mol Cell Med. 2015;4(1):1-8.

Membrane/protein trafficking in the secretory/biosynthetic and endocytic pathways is mediated by vesicles. Vesicle trafficking in eukaryotes is regulated by a class of small monomeric GTPases: the Rab protein family. Rab proteins represent the largest branch of the Ras superfamily...

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Bhuin T, Roy JK. Rab11 in disease progression. Int J Mol Cell Med. 2015;4(1):1-8
Bhuin, T., & Roy, J. K. (2015). Rab11 in disease progression. International journal of molecular and cellular medicine, 4(1), 1-8.
Bhuin, Tanmay, and Roy, Jagat Kumar. "Rab11 in disease progression." International journal of molecular and cellular medicine vol. 4,1 (2015): 1-8.
Bhuin T, Roy JK. Rab11 in disease progression. Int J Mol Cell Med. 2015;4(1):1-8. PMID: 25815277; PMCID: PMC4359700.
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Structural basis for targeting BIG1 to Golgi apparatus through interaction of its DCB domain with Arl1.

Journal of molecular cell biology

Wang R, Wang Z, Wang K, Zhang T, Ding J.
PMID: 27436755
J Mol Cell Biol. 2016 Oct 01;8(5):459-461. doi: 10.1093/jmcb/mjw033.

No abstract available.

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Wang R, Wang Z, Wang K, et al. Structural basis for targeting BIG1 to Golgi apparatus through interaction of its DCB domain with Arl1. J Mol Cell Biol. 2016;8(5):459-461doi: 10.1093/jmcb/mjw033.
Wang, R., Wang, Z., Wang, K., Zhang, T., & Ding, J. (2016). Structural basis for targeting BIG1 to Golgi apparatus through interaction of its DCB domain with Arl1. Journal of molecular cell biology, 8(5), 459-461. https://doi.org/10.1093/jmcb/mjw033
Wang, Rong, et al. "Structural basis for targeting BIG1 to Golgi apparatus through interaction of its DCB domain with Arl1." Journal of molecular cell biology vol. 8,5 (2016): 459-461. doi: https://doi.org/10.1093/jmcb/mjw033
Wang R, Wang Z, Wang K, Zhang T, Ding J. Structural basis for targeting BIG1 to Golgi apparatus through interaction of its DCB domain with Arl1. J Mol Cell Biol. 2016 Oct 01;8(5):459-461. doi: 10.1093/jmcb/mjw033. PMID: 27436755.
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The Frequency of Exotoxin A and Exoenzymes S and U Genes Among Clinical Isolates of Pseudomonas aeruginosa in Shiraz, Iran.

International journal of molecular and cellular medicine

Yousefi-Avarvand A, Khashei R, Sedigh Ebrahim-Saraie H, Emami A, Zomorodian K, Motamedifar M.
PMID: 26629485
Int J Mol Cell Med. 2015;4(3):167-73.

Pseudomonas aeruginosa as an opportunistic pathogen produces several virulence factors. The most important of these factors are exotoxin A and type III secretion system (T3SS). The aim of this study was to determine the frequency of toxA, exoU and...

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Yousefi-Avarvand A, Khashei R, Sedigh Ebrahim-Saraie H, et al. The Frequency of Exotoxin A and Exoenzymes S and U Genes Among Clinical Isolates of Pseudomonas aeruginosa in Shiraz, Iran. Int J Mol Cell Med. 2015;4(3):167-73
Yousefi-Avarvand, A., Khashei, R., Sedigh Ebrahim-Saraie, H., Emami, A., Zomorodian, K., & Motamedifar, M. (2015). The Frequency of Exotoxin A and Exoenzymes S and U Genes Among Clinical Isolates of Pseudomonas aeruginosa in Shiraz, Iran. International journal of molecular and cellular medicine, 4(3), 167-73.
Yousefi-Avarvand, Arshid, et al. "The Frequency of Exotoxin A and Exoenzymes S and U Genes Among Clinical Isolates of Pseudomonas aeruginosa in Shiraz, Iran." International journal of molecular and cellular medicine vol. 4,3 (2015): 167-73.
Yousefi-Avarvand A, Khashei R, Sedigh Ebrahim-Saraie H, Emami A, Zomorodian K, Motamedifar M. The Frequency of Exotoxin A and Exoenzymes S and U Genes Among Clinical Isolates of Pseudomonas aeruginosa in Shiraz, Iran. Int J Mol Cell Med. 2015;4(3):167-73. PMID: 26629485; PMCID: PMC4644528.
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The role of hypoxia in intestinal inflammation.

Molecular and cellular pediatrics

Shah YM.
PMID: 26812949
Mol Cell Pediatr. 2016 Dec;3(1):1. doi: 10.1186/s40348-016-0030-1. Epub 2016 Jan 26.

Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory disease of the intestine. IBD is a multifactorial disorder, and IBD-associated genes are critical in innate immune response, inflammatory response, autophagy, and epithelial barrier integrity. Moreover, epithelial oxygen tension plays...

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Shah YM. The role of hypoxia in intestinal inflammation. Mol Cell Pediatr. 2016;3(1):1doi: 10.1186/s40348-016-0030-1.
Shah, Y. M. (2016). The role of hypoxia in intestinal inflammation. Molecular and cellular pediatrics, 3(1), 1. https://doi.org/10.1186/s40348-016-0030-1
Shah, Yatrik M. "The role of hypoxia in intestinal inflammation." Molecular and cellular pediatrics vol. 3,1 (2016): 1. doi: https://doi.org/10.1186/s40348-016-0030-1
Shah YM. The role of hypoxia in intestinal inflammation. Mol Cell Pediatr. 2016 Dec;3(1):1. doi: 10.1186/s40348-016-0030-1. Epub 2016 Jan 26. PMID: 26812949; PMCID: PMC4728161.
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Analysis of Copy Number Variations in Patients with Autism Using Cytogenetic and MLPA Techniques: Report of 16p13.1p13.3 and 10q26.3 Duplications.

International journal of molecular and cellular medicine

Ghasemi Firouzabadi S, Vameghi R, Kariminejad R, Darvish H, Banihashemi S, Firouzkouhi Moghaddam M, Jamali P, Farbod Mofidi Tehrani H, Dehghani H, Raeisoon MR, Narooie-Nejad M, Jamshidi J, Tafakhori A, Sadabadi S, Behjati F.
PMID: 28357200
Int J Mol Cell Med. 2016;5(4):236-245. Epub 2016 Dec 05.

Autism is a common neuropsychiatric disorder affecting 1 in 68 children. Copy number variations (CNVs) are known to be major contributors of autism spectrum disorder (ASD). There are different whole genome or targeted techniques to identify CNVs in the...

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Ghasemi Firouzabadi S, Vameghi R, Kariminejad R, et al. Analysis of Copy Number Variations in Patients with Autism Using Cytogenetic and MLPA Techniques: Report of 16p13.1p13.3 and 10q26.3 Duplications. Int J Mol Cell Med. 2016;5(4):236-245
Ghasemi Firouzabadi, S., Vameghi, R., Kariminejad, R., Darvish, H., Banihashemi, S., Firouzkouhi Moghaddam, M., Jamali, P., Farbod Mofidi Tehrani, H., Dehghani, H., Raeisoon, M. R., Narooie-Nejad, M., Jamshidi, J., Tafakhori, A., Sadabadi, S., & Behjati, F. (2016). Analysis of Copy Number Variations in Patients with Autism Using Cytogenetic and MLPA Techniques: Report of 16p13.1p13.3 and 10q26.3 Duplications. International journal of molecular and cellular medicine, 5(4), 236-245.
Ghasemi Firouzabadi, Saghar, et al. "Analysis of Copy Number Variations in Patients with Autism Using Cytogenetic and MLPA Techniques: Report of 16p13.1p13.3 and 10q26.3 Duplications." International journal of molecular and cellular medicine vol. 5,4 (2016): 236-245.
Ghasemi Firouzabadi S, Vameghi R, Kariminejad R, Darvish H, Banihashemi S, Firouzkouhi Moghaddam M, Jamali P, Farbod Mofidi Tehrani H, Dehghani H, Raeisoon MR, Narooie-Nejad M, Jamshidi J, Tafakhori A, Sadabadi S, Behjati F. Analysis of Copy Number Variations in Patients with Autism Using Cytogenetic and MLPA Techniques: Report of 16p13.1p13.3 and 10q26.3 Duplications. Int J Mol Cell Med. 2016;5(4):236-245. Epub 2016 Dec 05. PMID: 28357200; PMCID: PMC5353985.
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