192,209 Works

Additional file 7: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S7. Effects of ruxolitinib on pSTAT5 and tumor latency. (A) Serum prolactin levels of mice. (B) Immunohistochemistry analysis and the accompanying dot plot for pSTAT5+ cells. The p values were determined using the Mann-Whitney test. Each dot in this plot represents one mouse. (C) Kaplan-Meier tumor-free survival curve of mice infected by RCAS-HRasQ61L. The p value was determined by generalized Gehan-Wilcoxon test with Rhoâ =â 1. (AI 6247 kb)

Additional file 7: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S7. Effects of ruxolitinib on pSTAT5 and tumor latency. (A) Serum prolactin levels of mice. (B) Immunohistochemistry analysis and the accompanying dot plot for pSTAT5+ cells. The p values were determined using the Mann-Whitney test. Each dot in this plot represents one mouse. (C) Kaplan-Meier tumor-free survival curve of mice infected by RCAS-HRasQ61L. The p value was determined by generalized Gehan-Wilcoxon test with Rhoâ =â 1. (AI 6247 kb)

Additional file 6: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S6. Effects of genetic ablation of STAT5a on downstream factors of STAT5. Immunohistochemistry analysis of β-casein in caErbB2 early lesions. (AI 4570 kb)

Additional file 6: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S6. Effects of genetic ablation of STAT5a on downstream factors of STAT5. Immunohistochemistry analysis of β-casein in caErbB2 early lesions. (AI 4570 kb)

Additional file 5: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S5. Effects of aripiprazole and clomipramine on biomarkers and lesion burden. (A) Serum prolactin levels of mice in the aripiprazole study. (B) Lesion burden determined by immunohistochemical staining for the HA tag on RCAS-caErbB2. (C) Ki67+ cells determined by immunofluorescence staining. (D) TUNEL+ cells. (E) Serum prolactin levels of mice in the clomipramine study. (F) Lesion burden determined by immunohistochemical staining for the HA tag on RCAS-caErbB2. The p values were determined using the...

Additional file 5: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S5. Effects of aripiprazole and clomipramine on biomarkers and lesion burden. (A) Serum prolactin levels of mice in the aripiprazole study. (B) Lesion burden determined by immunohistochemical staining for the HA tag on RCAS-caErbB2. (C) Ki67+ cells determined by immunofluorescence staining. (D) TUNEL+ cells. (E) Serum prolactin levels of mice in the clomipramine study. (F) Lesion burden determined by immunohistochemical staining for the HA tag on RCAS-caErbB2. The p values were determined using the...

Additional file 4: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S4. Pimozide accelerates the development of early lesions initiated by RCAS-caErbB2 while lowering the anticancer barrier of apoptosis. (A) Immunohistochemical staining for the HA tag on the RCAS-ErbB2 provirus with the corresponding dot plot. (B) Immunofluorescence staining for Ki67 with the accompanying dot plot. (C and D) Immunofluorescence staining for cleaved caspase 3 (C) and TUNEL assay (D) with the accompanying dot plots. The Mann-Whitney test was used to determine the p values. Each...

Additional file 4: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S4. Pimozide accelerates the development of early lesions initiated by RCAS-caErbB2 while lowering the anticancer barrier of apoptosis. (A) Immunohistochemical staining for the HA tag on the RCAS-ErbB2 provirus with the corresponding dot plot. (B) Immunofluorescence staining for Ki67 with the accompanying dot plot. (C and D) Immunofluorescence staining for cleaved caspase 3 (C) and TUNEL assay (D) with the accompanying dot plots. The Mann-Whitney test was used to determine the p values. Each...

Additional file 3: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S3. Pimozide increases serum prolactin levels, pSTAT5 in early lesions, and β-casein, while aripiprazole does not impact pSTAT5. (A) Serum prolactin levels. (B) pSTAT5+ cells determined by immunohistochemistry analysis. (C) Immunohistochemistry analysis of β-casein. (D) pSTAT5+ cells determined by immunohistochemistry analysis. The p values were determined using the Mann-Whitney test. Each dot in these plots represents one mouse. (AI 6764 kb)

Additional file 3: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S3. Pimozide increases serum prolactin levels, pSTAT5 in early lesions, and β-casein, while aripiprazole does not impact pSTAT5. (A) Serum prolactin levels. (B) pSTAT5+ cells determined by immunohistochemistry analysis. (C) Immunohistochemistry analysis of β-casein. (D) pSTAT5+ cells determined by immunohistochemistry analysis. The p values were determined using the Mann-Whitney test. Each dot in these plots represents one mouse. (AI 6764 kb)

Additional file 2: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S2. Risperidone treatment accelerates early lesion development of MMTV-Wnt1 transgenic mice. (A) Carmine whole mount staining of mammary glands from MMTV-Wnt1 transgenic mice. (B) H&E staining of mammary gland sections of MMTV-Wnt1 mice. (C) pSTAT5 immunohistochemical staining of mammary gland sections of MMTV-Wnt1 mice. (AI 22593 kb)

Additional file 2: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S2. Risperidone treatment accelerates early lesion development of MMTV-Wnt1 transgenic mice. (A) Carmine whole mount staining of mammary glands from MMTV-Wnt1 transgenic mice. (B) H&E staining of mammary gland sections of MMTV-Wnt1 mice. (C) pSTAT5 immunohistochemical staining of mammary gland sections of MMTV-Wnt1 mice. (AI 22593 kb)

Additional file 1: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S1. Risperidone treatment does not affect tumor histopathology or lung metastatic potential. (A) H&E staining of tumor sections. (B) qPCR analysis of lung metastasis and the resulting dot plot analyzed using the Mann-Whitney test. Each dot in this plot represents one mouse. (AI 4884 kb)

Additional file 1: of Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions

A. Johnston, W. Bu, S. Hein, S. Garcia, L. Camacho, L. Xue, L. Qin, C. Nagi, S. Hilsenbeck, J. Kapali, K. Podsypanina, J. Nangia & Y. Li
Figure S1. Risperidone treatment does not affect tumor histopathology or lung metastatic potential. (A) H&E staining of tumor sections. (B) qPCR analysis of lung metastasis and the resulting dot plot analyzed using the Mann-Whitney test. Each dot in this plot represents one mouse. (AI 4884 kb)

Hindlimb Loading by Experimental Group

Adam Foster
Boxplot of the average amount of load (as a percentage of body mass), experienced by the hindlimbs over a 60 minute exercise period in each experimental group, over a twelve week experiment. All comparisons are significantly different (p<0.001).

Rat Body Masses over the 12-Week Experiment

Adam Foster
Barplot of rat body masses by group over the course of the 12-week experiment. Error bars are the standard error (SE).

Abnormal BDNF signalling underscores defects of cerebellar development in a mouse model of Niemann-Pick type C1 disease

Francesco Bruno
The Niemann-Pick type C1 (NPC1) disease is a lysosomal storage disorder caused by defective intracellular trafficking of exogenous cholesterol. This causes, among others, a depletion of cholesterol in lipid rafts, likely impairing various signal transduction pathways. Therapies based on hydroxy-propyl-beta-cyclodextrins (HPBCD) administration represent at the moment the most promising approach.
Studying the early postnatal cerebellum development in a mouse model of NPC1 disease, we have observed: i) a reduced proliferation of granule neuron precursors;...

Abnormal BDNF signalling underscores defects of cerebellar development in a mouse model of Niemann-Pick type C1 disease

Francesco Bruno
The Niemann-Pick type C1 (NPC1) disease is a lysosomal storage disorder caused by defective intracellular trafficking of exogenous cholesterol. This causes, among others, a depletion of cholesterol in lipid rafts, likely impairing various signal transduction pathways. Therapies based on hydroxy-propyl-beta-cyclodextrins (HPBCD) administration represent at the moment the most promising approach.
Studying the early postnatal cerebellum development in a mouse model of NPC1 disease, we have observed: i) a reduced proliferation of granule neuron precursors;...

Additional file 3: of Myeloid-specific TAK1 deletion results in reduced brain monocyte infiltration and improved outcomes after stroke

Anjali Chauhan, Jacob Hudobenko, Abdullah Al Mamun, Edward Koellhoffer, Anthony Patrizz, Rodney Ritzel, Bhanu Ganesh & Louise McCullough
Figure S3. mRNA expression of TAK1 in micro glia isolated from mouse brain. Microglia from the brain of WT and TAK1ΔM mice were isolated by cell sorting. Isolated cells were treated with RNA later. Extracted mRNA (3 μg) from the microglia population were converted to cDNA. The expression levels of the target genes were calculated with the relative standard curve method after normalizing the target gene expression to the expression of the house-keeping gene encoding glyceraldehyde...

Additional file 3: of Myeloid-specific TAK1 deletion results in reduced brain monocyte infiltration and improved outcomes after stroke

Anjali Chauhan, Jacob Hudobenko, Abdullah Al Mamun, Edward Koellhoffer, Anthony Patrizz, Rodney Ritzel, Bhanu Ganesh & Louise McCullough
Figure S3. mRNA expression of TAK1 in micro glia isolated from mouse brain. Microglia from the brain of WT and TAK1ΔM mice were isolated by cell sorting. Isolated cells were treated with RNA later. Extracted mRNA (3 μg) from the microglia population were converted to cDNA. The expression levels of the target genes were calculated with the relative standard curve method after normalizing the target gene expression to the expression of the house-keeping gene encoding glyceraldehyde...

Additional file 6: of Use of designed sequences in protein structure recognition

Gayatri Kumar, Richa Mudgal, Narayanaswamy Srinivasan & Sankaran Sandhya
Figure S4. False vs. True positives for queries in the assessment dataset: The distribution of true positives vs. false positives as a function of a) Query and target coverage. b) Query and target alignment length (number of residues in the alignment). (PNG 363 kb)

Additional file 2: of Myeloid-specific TAK1 deletion results in reduced brain monocyte infiltration and improved outcomes after stroke

Anjali Chauhan, Jacob Hudobenko, Abdullah Al Mamun, Edward Koellhoffer, Anthony Patrizz, Rodney Ritzel, Bhanu Ganesh & Louise McCullough
Figure S2. Large vessel anatomy and cerebral blood flow changes A. No gross anatomical difference in the large blood vessels between WT and TAK1ΔM naïve mice (n = 3). B. No difference in cerebral blood flow between WT and TAK1ΔM MCAo mice (n = 5). (JPG 35 kb)

Additional file 2: of Myeloid-specific TAK1 deletion results in reduced brain monocyte infiltration and improved outcomes after stroke

Anjali Chauhan, Jacob Hudobenko, Abdullah Al Mamun, Edward Koellhoffer, Anthony Patrizz, Rodney Ritzel, Bhanu Ganesh & Louise McCullough
Figure S2. Large vessel anatomy and cerebral blood flow changes A. No gross anatomical difference in the large blood vessels between WT and TAK1ΔM naïve mice (n = 3). B. No difference in cerebral blood flow between WT and TAK1ΔM MCAo mice (n = 5). (JPG 35 kb)

Additional file 6: of Use of designed sequences in protein structure recognition

Gayatri Kumar, Richa Mudgal, Narayanaswamy Srinivasan & Sankaran Sandhya
Figure S4. False vs. True positives for queries in the assessment dataset: The distribution of true positives vs. false positives as a function of a) Query and target coverage. b) Query and target alignment length (number of residues in the alignment). (PNG 363 kb)

Additional file 5: of Use of designed sequences in protein structure recognition

Gayatri Kumar, Richa Mudgal, Narayanaswamy Srinivasan & Sankaran Sandhya
Figure S3. The normalized fold frequency of correct vs. incorrect associations for the assessment dataset: The preponderance of ‘correct’ associated folds (in green) is observed at a higher normalized fold frequency than other ‘incorrect’ fold associations (in red). (PNG 92 kb)

Resource Types

  • Image
    192,209

Publication Year

  • 2018
    8,658
  • 2017
    16,902
  • 2016
    14,652
  • 2015
    7,880
  • 2014
    3,305
  • 2013
    4,480
  • 2012
    1,440
  • 2011
    134,892

Registration Year

  • 2018
    8,711
  • 2017
    23,910
  • 2016
    86,083
  • 2015
    1,678
  • 2014
    2,602
  • 2013
    2,214
  • 2012
    67,011