cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.13114712
title: Additional file 5 of Identification of loci and candidate gene GmSPX-RING1 responsible for phosphorus efficiency in soybean via genome-wide association analysis

description: Additional file 5: Table S2. Details of SNPs significantly associated with two P efficiency-related traits in only one hydroponic experiments. SDWP: shoot dry weight under +P condition, SDWM: shoot dry weight under -P condition, SDWR: the ratio of shoot dry weight under -P condition to +P condition; SPP: shoot P concentration under +P condition, SPM: shoot P concentration under -P condition, SPR: the ratio of shoot P concentration under -P condition to +P condition; SPAP: shoot P accumulation under +P condition, SPAM: shoot P accumulation under -P condition, SPAR: the ratio of shoot P accumulation under -P condition to +P condition. Chr.: chromosome; P value: significant at P ≤ 4.82 × 10− 6; R2: percentage of phenotypic variation explained by the SNP; Exp.: experiment; E1/E2: first/second independent hydroponic culture. Mean: average of the two experiments.
DOI: 10.6084/m9.figshare.20454760.v1
title: Additional file 1 of DNA damage repair gene signature model for predicting prognosis and chemotherapy outcomes in lung squamous cell carcinoma

description: Additional file 1: Table S1. Clinical information. Table S2. Marker For ssGSEA. Table S3. Prognosis related DNA repair genes. Table S4. Differently expressed genes.
DOI: 10.6084/m9.figshare.13114694
title: Additional file 11 of Identification of loci and candidate gene GmSPX-RING1 responsible for phosphorus efficiency in soybean via genome-wide association analysis

description: Additional file 11: Table S4. Primers used in this study.
DOI: 10.6084/m9.figshare.13114694.v1
title: Additional file 11 of Identification of loci and candidate gene GmSPX-RING1 responsible for phosphorus efficiency in soybean via genome-wide association analysis

description: Additional file 11: Table S4. Primers used in this study.
DOI: 10.6084/m9.figshare.13114731.v1
title: Additional file 8 of Transcriptomic and metabolomic profiling reveals the effect of LED light quality on morphological traits, and phenylpropanoid-derived compounds accumulation in Sarcandra glabra seedlings

description: Additional file 8: Table S5. Summary of identified genes and their FPKM values.
DOI: 10.6084/m9.figshare.13114703.v1
title: Additional file 2 of Identification of loci and candidate gene GmSPX-RING1 responsible for phosphorus efficiency in soybean via genome-wide association analysis

description: Additional file 2: Table S1. Correlation coefficients of three P-efficiency traits in natural population under two P conditions. SDW: shoot dry weight; SP: shoot P concentration; SPA: shoot P accumulation. The correlation coefficients of natural populations under +P (0.5 mM KH2PO4) and -P (0.005 mM KH2PO4) conditions were listed in the upper right and lower left of the table, respectively. ns: not significant; *, **and *** significant at 0.05, 0.01 and 0.001 probability levels, respectively.
DOI: 10.6084/m9.figshare.13114734
title: Additional file 9 of Transcriptomic and metabolomic profiling reveals the effect of LED light quality on morphological traits, and phenylpropanoid-derived compounds accumulation in Sarcandra glabra seedlings

description: Additional file 9: Table S6. The transcript sequences of the selected genes.
DOI: 10.6084/m9.figshare.13114734.v1
title: Additional file 9 of Transcriptomic and metabolomic profiling reveals the effect of LED light quality on morphological traits, and phenylpropanoid-derived compounds accumulation in Sarcandra glabra seedlings

description: Additional file 9: Table S6. The transcript sequences of the selected genes.
DOI: 10.6084/m9.figshare.13114691
title: Additional file 10 of Identification of loci and candidate gene GmSPX-RING1 responsible for phosphorus efficiency in soybean via genome-wide association analysis

description: Additional file 10: Table S3. Geographic origins of 211 soybean accessions.
DOI: 10.6084/m9.figshare.13114731
title: Additional file 8 of Transcriptomic and metabolomic profiling reveals the effect of LED light quality on morphological traits, and phenylpropanoid-derived compounds accumulation in Sarcandra glabra seedlings

description: Additional file 8: Table S5. Summary of identified genes and their FPKM values.
DOI: 10.6084/m9.figshare.9969050
title: MOESM2 of In vivo immobilization of an organophosphorus hydrolyzing enzyme on bacterial polyhydroxyalkanoate nano-granules

description: Additional file 2. Protein groups.
DOI: 10.6084/m9.figshare.9969050.v1
title: MOESM2 of In vivo immobilization of an organophosphorus hydrolyzing enzyme on bacterial polyhydroxyalkanoate nano-granules

description: Additional file 2. Protein groups.
DOI: 10.6084/m9.figshare.9969152
title: MOESM1 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 1: Table S1. The significant enrichment GO terms at 6â h, 24â h, and 72â h. (XLSX 21 kb)
DOI: 10.6084/m9.figshare.9969152.v1
title: MOESM1 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 1: Table S1. The significant enrichment GO terms at 6â h, 24â h, and 72â h. (XLSX 21 kb)
DOI: 10.6084/m9.figshare.9969155
title: MOESM2 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 2: Table S2. The significant enrichment KEGG pathway at 6â h, 24â h, and 72â h. (XLSX 16 kb)
DOI: 10.6084/m9.figshare.9969155.v1
title: MOESM2 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 2: Table S2. The significant enrichment KEGG pathway at 6â h, 24â h, and 72â h. (XLSX 16 kb)
DOI: 10.6084/m9.figshare.9969158
title: MOESM1 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 1: Table S1. A complete list of all the proteins identified in this study.
DOI: 10.6084/m9.figshare.9969158.v1
title: MOESM1 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 1: Table S1. A complete list of all the proteins identified in this study.
DOI: 10.6084/m9.figshare.9969164
title: MOESM2 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 2: Table S2. The acquired raw files were analyzed by Maxquant. List of 12 proteins differentially expression by PC-1.0 and PC-1 pancreatic cancer cells with fold changeâ &gt;â 1.5.
DOI: 10.6084/m9.figshare.9969164.v1
title: MOESM2 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 2: Table S2. The acquired raw files were analyzed by Maxquant. List of 12 proteins differentially expression by PC-1.0 and PC-1 pancreatic cancer cells with fold changeâ &gt;â 1.5.
DOI: 10.6084/m9.figshare.7872014
title: GORASP2/GRASP55 collaborates with the PtdIns3K UVRAG complex to facilitate autophagosome-lysosome fusion

description: It has been indicated that the Golgi apparatus contributes to autophagy, but how it is involved in autophagosome formation and maturation is not well understood. Here we show that amino acid starvation causes <i>trans</i>-Golgi derived membrane fragments to colocalize with autophagosomes. Depletion of the Golgi stacking protein GORASP2/GRASP55, but not GORASP1/GRASP65, increases both MAP1LC3 (LC3)-II and SQSTM1/p62 levels. We demonstrate that GORASP2 facilitates autophagosome-lysosome fusion by physically linking autophagosomes and lysosomes through the interactions with LC3 on autophagosomes and LAMP2 on late endosomes/lysosomes. Furthermore, we provide evidence that GORASP2 interacts with BECN1 to facilitate the assembly and membrane association of the phosphatidylinositol 3-kinase (PtdIns3K) UVRAG complex. These findings indicate that GORASP2 plays an important role in autophagosome maturation during amino acid starvation. ATG14: autophagy related 14; BafA1: bafilomycin A<sub>1</sub>; BSA: bovine serum albumin; CQ: chloroquine; EBSS: earle’s balanced salt solution; EM: electron microscopy; EEA1: early endosome antigen 1; GFP: green fluorescent protein; GORASP1/GRASP65: golgi reassembly stacking protein 1; GORASP2/GRASP55: golgi reassembly stacking protein 2; LAMP1: lysosomal-associated membrane protein 1; LAMP2: lysosomal-associated membrane protein 2; MAP1LC3: microtubule associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; PBS: phosphate-buffered saline; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol 3-phosphate; PK: protease K; PNS: post-nuclear supernatant; RFP: red fluorescent protein; SD: standard deviation; TGN: trans-Golgi network; UVRAG: UV radiation resistance associated.
DOI: 10.6084/m9.figshare.7872014.v2
title: GORASP2/GRASP55 collaborates with the PtdIns3K UVRAG complex to facilitate autophagosome-lysosome fusion

description: It has been indicated that the Golgi apparatus contributes to autophagy, but how it is involved in autophagosome formation and maturation is not well understood. Here we show that amino acid starvation causes <i>trans</i>-Golgi derived membrane fragments to colocalize with autophagosomes. Depletion of the Golgi stacking protein GORASP2/GRASP55, but not GORASP1/GRASP65, increases both MAP1LC3 (LC3)-II and SQSTM1/p62 levels. We demonstrate that GORASP2 facilitates autophagosome-lysosome fusion by physically linking autophagosomes and lysosomes through the interactions with LC3 on autophagosomes and LAMP2 on late endosomes/lysosomes. Furthermore, we provide evidence that GORASP2 interacts with BECN1 to facilitate the assembly and membrane association of the phosphatidylinositol 3-kinase (PtdIns3K) UVRAG complex. These findings indicate that GORASP2 plays an important role in autophagosome maturation during amino acid starvation. ATG14: autophagy related 14; BafA1: bafilomycin A<sub>1</sub>; BSA: bovine serum albumin; CQ: chloroquine; EBSS: earle’s balanced salt solution; EM: electron microscopy; EEA1: early endosome antigen 1; GFP: green fluorescent protein; GORASP1/GRASP65: golgi reassembly stacking protein 1; GORASP2/GRASP55: golgi reassembly stacking protein 2; LAMP1: lysosomal-associated membrane protein 1; LAMP2: lysosomal-associated membrane protein 2; MAP1LC3: microtubule associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; PBS: phosphate-buffered saline; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol 3-phosphate; PK: protease K; PNS: post-nuclear supernatant; RFP: red fluorescent protein; SD: standard deviation; TGN: trans-Golgi network; UVRAG: UV radiation resistance associated.
DOI: 10.6084/m9.figshare.7872014.v1
title: GORASP2/GRASP55 collaborates with the PtdIns3K UVRAG complex to facilitate autophagosome-lysosome fusion

description: It has been indicated that the Golgi apparatus contributes to autophagy, but how it is involved in autophagosome formation and maturation is not well understood. Here we show that amino acid starvation causes <i>trans</i>-Golgi derived membrane fragments to colocalize with autophagosomes. Depletion of the Golgi stacking protein GORASP2/GRASP55, but not GORASP1/GRASP65, increases both MAP1LC3 (LC3)-II and SQSTM1/p62 levels. We demonstrate that GORASP2 facilitates autophagosome-lysosome fusion by physically linking autophagosomes and lysosomes through the interactions with LC3 on autophagosomes and LAMP2 on late endosomes/lysosomes. Furthermore, we provide evidence that GORASP2 interacts with BECN1 to facilitate the assembly and membrane association of the phosphatidylinositol 3-kinase (PtdIns3K) UVRAG complex. These findings indicate that GORASP2 plays an important role in autophagosome maturation during amino acid starvation.
DOI: 10.6084/m9.figshare.7872017
title: Impaired TFEB-mediated lysosomal biogenesis promotes the development of pancreatitis in mice and is associated with human pancreatitis

description: Impaired macroautophagy/autophagy has been implicated in experimental and human pancreatitis. However, the transcriptional control governing the autophagy-lysosomal process in pancreatitis is largely unknown. We investigated the role and mechanisms of TFEB (transcription factor EB), a master regulator of lysosomal biogenesis, in the pathogenesis of experimental pancreatitis. We analyzed autophagic flux, TFEB nuclear translocation, lysosomal biogenesis, inflammation and fibrosis in GFP-LC3 transgenic mice, acinar cell-specific <i>tfeb</i> knockout (KO) and <i>tfeb</i> and <i>tfe3</i> double-knockout (DKO) mice as well as human pancreatitis samples. We found that cerulein activated MTOR (mechanistic target of rapamycin kinase) and increased the levels of phosphorylated TFEB as well as pancreatic proteasome activities that led to rapid TFEB degradation. As a result, cerulein decreased the number of lysosomes resulting in insufficient autophagy in mouse pancreas. Pharmacological inhibition of MTOR or proteasome partially rescued cerulein-induced TFEB degradation and pancreatic damage. Furthermore, genetic deletion of <i>tfeb</i> specifically in mouse pancreatic acinar cells increased pancreatic edema, necrotic cell death, infiltration of inflammatory cells and fibrosis in pancreas after cerulein treatment. <i>tfeb</i> and <i>tfe3</i> DKO mice also developed spontaneous pancreatitis with increased pancreatic trypsin activities, edema and infiltration of inflammatory cells. Finally, decreased TFEB nuclear staining was associated with human pancreatitis. In conclusion, our results indicate a critical role of impaired TFEB-mediated lysosomal biogenesis in promoting the pathogenesis of pancreatitis. <b>Abbreviations:</b> AC: acinar cell; AMY: amylase; ATP6V1A: ATPase, H+ transporting, lysosomal V1 subunit A; ATP6V1B2: ATPase, H+ transporting, lysosomal V1 subunit B2; ATP6V1D: ATPase, H+ transporting, lysosomal V1 subunit D; ATP6V1H: ATPase, H+ transporting, lysosomal V1 subunit H; AV: autophagic vacuole; CDE: choline-deficient, ethionine-supplemented; CLEAR: coordinated lysosomal expression and regulation; CQ: chloroquine; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; EM: electron microscopy; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; H & E: hematoxylin and eosin; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK1/ERK2: mitogen-activated protein kinase 1; MTORC1: mechanistic target of rapamycin kinase complex 1; ND: normal donor; NEU: neutrophil; PPARGC1A/PGC1α: peroxisome proliferator-activated receptor, gamma, coactivator 1 alpha; RIPA: radio-immunoprecipitation; RPS6: ribosomal protein S6; SQSTM1/p62: sequestosome 1; TFEB: transcription factor EB; TM: tamoxifen; WT: wild-type; ZG: zymogen granule
DOI: 10.6084/m9.figshare.7872017.v2
title: Impaired TFEB-mediated lysosomal biogenesis promotes the development of pancreatitis in mice and is associated with human pancreatitis

description: Impaired macroautophagy/autophagy has been implicated in experimental and human pancreatitis. However, the transcriptional control governing the autophagy-lysosomal process in pancreatitis is largely unknown. We investigated the role and mechanisms of TFEB (transcription factor EB), a master regulator of lysosomal biogenesis, in the pathogenesis of experimental pancreatitis. We analyzed autophagic flux, TFEB nuclear translocation, lysosomal biogenesis, inflammation and fibrosis in GFP-LC3 transgenic mice, acinar cell-specific <i>tfeb</i> knockout (KO) and <i>tfeb</i> and <i>tfe3</i> double-knockout (DKO) mice as well as human pancreatitis samples. We found that cerulein activated MTOR (mechanistic target of rapamycin kinase) and increased the levels of phosphorylated TFEB as well as pancreatic proteasome activities that led to rapid TFEB degradation. As a result, cerulein decreased the number of lysosomes resulting in insufficient autophagy in mouse pancreas. Pharmacological inhibition of MTOR or proteasome partially rescued cerulein-induced TFEB degradation and pancreatic damage. Furthermore, genetic deletion of <i>tfeb</i> specifically in mouse pancreatic acinar cells increased pancreatic edema, necrotic cell death, infiltration of inflammatory cells and fibrosis in pancreas after cerulein treatment. <i>tfeb</i> and <i>tfe3</i> DKO mice also developed spontaneous pancreatitis with increased pancreatic trypsin activities, edema and infiltration of inflammatory cells. Finally, decreased TFEB nuclear staining was associated with human pancreatitis. In conclusion, our results indicate a critical role of impaired TFEB-mediated lysosomal biogenesis in promoting the pathogenesis of pancreatitis. <b>Abbreviations:</b> AC: acinar cell; AMY: amylase; ATP6V1A: ATPase, H+ transporting, lysosomal V1 subunit A; ATP6V1B2: ATPase, H+ transporting, lysosomal V1 subunit B2; ATP6V1D: ATPase, H+ transporting, lysosomal V1 subunit D; ATP6V1H: ATPase, H+ transporting, lysosomal V1 subunit H; AV: autophagic vacuole; CDE: choline-deficient, ethionine-supplemented; CLEAR: coordinated lysosomal expression and regulation; CQ: chloroquine; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; EM: electron microscopy; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; H & E: hematoxylin and eosin; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK1/ERK2: mitogen-activated protein kinase 1; MTORC1: mechanistic target of rapamycin kinase complex 1; ND: normal donor; NEU: neutrophil; PPARGC1A/PGC1α: peroxisome proliferator-activated receptor, gamma, coactivator 1 alpha; RIPA: radio-immunoprecipitation; RPS6: ribosomal protein S6; SQSTM1/p62: sequestosome 1; TFEB: transcription factor EB; TM: tamoxifen; WT: wild-type; ZG: zymogen granule
DOI: 10.6084/m9.figshare.7872017.v3
title: Impaired TFEB-mediated lysosomal biogenesis promotes the development of pancreatitis in mice and is associated with human pancreatitis

description: Impaired macroautophagy/autophagy has been implicated in experimental and human pancreatitis. However, the transcriptional control governing the autophagy-lysosomal process in pancreatitis is largely unknown. We investigated the role and mechanisms of TFEB (transcription factor EB), a master regulator of lysosomal biogenesis, in the pathogenesis of experimental pancreatitis. We analyzed autophagic flux, TFEB nuclear translocation, lysosomal biogenesis, inflammation and fibrosis in GFP-LC3 transgenic mice, acinar cell-specific <i>tfeb</i> knockout (KO) and <i>tfeb</i> and <i>tfe3</i> double-knockout (DKO) mice as well as human pancreatitis samples. We found that cerulein activated MTOR (mechanistic target of rapamycin kinase) and increased the levels of phosphorylated TFEB as well as pancreatic proteasome activities that led to rapid TFEB degradation. As a result, cerulein decreased the number of lysosomes resulting in insufficient autophagy in mouse pancreas. Pharmacological inhibition of MTOR or proteasome partially rescued cerulein-induced TFEB degradation and pancreatic damage. Furthermore, genetic deletion of <i>tfeb</i> specifically in mouse pancreatic acinar cells increased pancreatic edema, necrotic cell death, infiltration of inflammatory cells and fibrosis in pancreas after cerulein treatment. <i>tfeb</i> and <i>tfe3</i> DKO mice also developed spontaneous pancreatitis with increased pancreatic trypsin activities, edema and infiltration of inflammatory cells. Finally, decreased TFEB nuclear staining was associated with human pancreatitis. In conclusion, our results indicate a critical role of impaired TFEB-mediated lysosomal biogenesis in promoting the pathogenesis of pancreatitis. <b>Abbreviations:</b> AC: acinar cell; AMY: amylase; ATP6V1A: ATPase, H+ transporting, lysosomal V1 subunit A; ATP6V1B2: ATPase, H+ transporting, lysosomal V1 subunit B2; ATP6V1D: ATPase, H+ transporting, lysosomal V1 subunit D; ATP6V1H: ATPase, H+ transporting, lysosomal V1 subunit H; AV: autophagic vacuole; CDE: choline-deficient, ethionine-supplemented; CLEAR: coordinated lysosomal expression and regulation; CQ: chloroquine; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; EM: electron microscopy; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; H & E: hematoxylin and eosin; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK1/ERK2: mitogen-activated protein kinase 1; MTORC1: mechanistic target of rapamycin kinase complex 1; ND: normal donor; NEU: neutrophil; PPARGC1A/PGC1α: peroxisome proliferator-activated receptor, gamma, coactivator 1 alpha; RIPA: radio-immunoprecipitation; RPS6: ribosomal protein S6; SQSTM1/p62: sequestosome 1; TFEB: transcription factor EB; TM: tamoxifen; WT: wild-type; ZG: zymogen granule
DOI: 10.6084/m9.figshare.9969167
title: MOESM3 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 3: Table S3. The annotation DEGs on plant hormone signal transduction pathway. (XLSX 15 kb)
DOI: 10.6084/m9.figshare.9969167.v1
title: MOESM3 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 3: Table S3. The annotation DEGs on plant hormone signal transduction pathway. (XLSX 15 kb)
DOI: 10.6084/m9.figshare.9969173
title: MOESM3 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 3: Table S3. GO term analysis of the identified proteins by DAVID.
DOI: 10.6084/m9.figshare.9969173.v1
title: MOESM3 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 3: Table S3. GO term analysis of the identified proteins by DAVID.
DOI: 10.6084/m9.figshare.9969176
title: MOESM4 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 4: Table S4. Genes related to antioxidant enzymes and ion transport. (XLSX 32 kb)
DOI: 10.6084/m9.figshare.9969176.v1
title: MOESM4 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 4: Table S4. Genes related to antioxidant enzymes and ion transport. (XLSX 32 kb)
DOI: 10.6084/m9.figshare.9969182
title: MOESM4 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 4: Table S4. String network coordinates.
DOI: 10.6084/m9.figshare.9969182.v1
title: MOESM4 of Differential secretome of pancreatic cancer cells in serum-containing conditioned medium reveals CCT8 as a new biomarker of pancreatic cancer invasion and metastasis

description: Additional file 4: Table S4. String network coordinates.
DOI: 10.6084/m9.figshare.9969185
title: MOESM5 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 5: Table S5. qRT-PCR primers. (XLSX 9 kb)
DOI: 10.6084/m9.figshare.9969185.v1
title: MOESM5 of RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

description: Additional files 5: Table S5. qRT-PCR primers. (XLSX 9 kb)