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  1. Article: Editorial: Placental physiology and placental derived stem cells for regenerative medicine.

    Kanaujiya, Jitendra K / Mishra, Jay S

    Frontiers in physiology

    2023  Volume 14, Page(s) 1346913

    Language English
    Publishing date 2023-12-14
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1346913
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Generation of Keratinocytes from Human Induced Pluripotent Stem Cells Under Defined Culture Conditions.

    Sah, Shyam Kishor / Kanaujiya, Jitendra K / Chen, I-Ping / Reichenberger, Ernst J

    Cellular reprogramming

    2020  Volume 23, Issue 1, Page(s) 1–13

    Abstract: Differentiation of keratinocytes from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) has become an important tool for wound healing research and for studying skin diseases in instances where patient cells are not ... ...

    Abstract Differentiation of keratinocytes from human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) has become an important tool for wound healing research and for studying skin diseases in instances where patient cells are not available. Several keratinocyte differentiation protocols using hiPSC colony fragments or embryoid bodies have been published with some requiring prolonged time for differentiation or extended use of reagent cocktails. In this study, we present a simplified method to efficiently generate large numbers of uniformly differentiated keratinocytes in less than 4 weeks from singularized hiPSCs with differentiation factors, retinoic acid and bone morphogenetic protein 4 (BMP4). Low seeding density of singularized iPSCs results in keratinocyte cultures with minimum cell death during differentiation and up to 96% homogeneity for keratin 14-positive cells and low percentage of keratinocyte maturation markers, comparable to early passage primary keratinocytes. hiPSC-derived keratinocytes remain in a proliferative state, can be maintained for prolonged periods of time, and can be terminally differentiated under high calcium conditions in the same way as primary human keratinocytes. Moreover, coculturing hiPSC-derived fibroblasts and keratinocytes consistently formed organotypic 3D skin equivalents. Therefore, keratinocytes generated by this method are a viable source of cells for downstream applications.
    MeSH term(s) Bone Morphogenetic Protein 4/metabolism ; Cell Culture Techniques/methods ; Cell Differentiation ; Cells, Cultured ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Human Embryonic Stem Cells/cytology ; Human Embryonic Stem Cells/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Keratinocytes/cytology ; Keratinocytes/metabolism ; Skin/cytology ; Skin/metabolism ; Tretinoin/metabolism
    Chemical Substances BMP4 protein, human ; Bone Morphogenetic Protein 4 ; Tretinoin (5688UTC01R)
    Language English
    Publishing date 2020-12-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2542436-1
    ISSN 2152-4998 ; 1557-7457 ; 2152-4971
    ISSN (online) 2152-4998 ; 1557-7457
    ISSN 2152-4971
    DOI 10.1089/cell.2020.0046
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    Zs.A 5452: Show issues Location:
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  3. Article ; Online: Genome-editing technologies and patent landscape overview.

    Benahmed-Miniuk, Fairouz / Kresz, Mat / Kanaujiya, Jitendra K / Southgate, Christopher D

    Pharmaceutical patent analyst

    2017  Volume 6, Issue 3, Page(s) 115–134

    Abstract: Unlike with zinc finger nuclease and transcriptional activator-like effector nuclease DNA modification technologies that rely on lead proteins, developed through expensive and time-consuming processes, the clustered regularly interspaced short ... ...

    Abstract Unlike with zinc finger nuclease and transcriptional activator-like effector nuclease DNA modification technologies that rely on lead proteins, developed through expensive and time-consuming processes, the clustered regularly interspaced short palindromic repeat (CRISPR)/Cas system has rapidly emerged as the most promising gene-editing technology to date for the modification of any selected DNA sequence. CRISPR is receiving tremendous fanfare due, in part, to its potential to provide a means to fundamentally alter medical genetics and especially cancer medicine. In this review, we compare key technologies of genome-editing zinc finger nucleases, transcriptional activator-like effector nucleases and CRISPR, with a focus on the race to acquire lucrative intellectual property rights, the current CRISPR patent dispute and potential repercussions on innovation and the adoption of this promising technology by the medical community.
    Language English
    Publishing date 2017-05
    Publishing country England
    Document type Journal Article
    ISSN 2046-8962
    ISSN (online) 2046-8962
    DOI 10.4155/ppa-2017-0004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Proteomic analysis of rosiglitazone and guggulsterone treated 3T3-L1 preadipocytes.

    Pal, Pooja / Kanaujiya, Jitendra K / Lochab, Savita / Tripathi, Shashi B / Sanyal, Sabyasachi / Behre, Gerhard / Trivedi, Arun K

    Molecular and cellular biochemistry

    2012  Volume 376, Issue 1-2, Page(s) 81–93

    Abstract: Adipogenesis is the differentiation of preadipocytes to adipocytes which is marked by the accumulation of lipid droplets. Adipogenic differentiation of 3T3-L1 cells is achieved by exposing the cells to Insulin, Dexamethasone and IBMX for 5-7 days. ... ...

    Abstract Adipogenesis is the differentiation of preadipocytes to adipocytes which is marked by the accumulation of lipid droplets. Adipogenic differentiation of 3T3-L1 cells is achieved by exposing the cells to Insulin, Dexamethasone and IBMX for 5-7 days. Thiazolidinedione drugs, like rosiglitazone are potent insulin sensitizing agents and have been shown to enhance lipid droplet formation in 3T3-L1 cells, a model cell line for preadipocyte differentiation. Guggulsterone is a natural drug extracted from the gum resin of tree Commiphora mukul. Guggulsterone has been shown to inhibit adipogenesis and induce apoptosis in 3T3-L1 cells. In this study we treated the 3T3-L1 preadipocytes with rosiglitazone and guggulsterone and assessed the protein expression profile using 2D gel electrophoresis-based proteomics to find out differential target proteins of these drugs. The proteins that were identified upon rosiglitazone treatment generally regulate cell proliferation and/or exhibit anti-inflammatory effect which strengthens its differentiation-inducing property. Guggulsterone treatment resulted in the identification of the apoptosis-inducing proteins to be up regulated which rightly is in agreement with the apoptosis-inducing property of guggulsterone in 3T3-L1 cells. Some of the proteins identified in our proteomic screen such as Galectin1, AnnexinA2 & TCTP were further confirmed by Real Time qPCR. Thus, the present study provides a better outlook of proteins being differentially regulated/expressed upon treatment with rosiglitazone and guggulsterone. The detailed study of the differentially expressed proteins identified in this proteomic screen may further provide the better molecular insight into the mode of action of these anti-diabetic drugs rosiglitazone and guggulsterone.
    MeSH term(s) 3T3-L1 Cells/drug effects ; 3T3-L1 Cells/metabolism ; Adipocytes/drug effects ; Adipocytes/metabolism ; Adipogenesis/drug effects ; Animals ; Annexin A2/genetics ; Annexin A2/metabolism ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Electrophoresis, Gel, Two-Dimensional/methods ; Galectin 1/genetics ; Galectin 1/metabolism ; Hypoglycemic Agents/pharmacology ; Mice ; Pregnenediones/pharmacology ; Proteomics/methods ; Real-Time Polymerase Chain Reaction ; Rosiglitazone ; Thiazolidinediones/pharmacology
    Chemical Substances Annexin A2 ; Biomarkers, Tumor ; Galectin 1 ; Hypoglycemic Agents ; Pregnenediones ; Thiazolidinediones ; tumor protein, translationally-controlled 1 ; Rosiglitazone (05V02F2KDG) ; pregna-4,17-diene-3,16-dione (A4PW148END)
    Language English
    Publishing date 2012-12-30
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 184833-1
    ISSN 1573-4919 ; 0300-8177
    ISSN (online) 1573-4919
    ISSN 0300-8177
    DOI 10.1007/s11010-012-1551-0
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 892: Show issues Location:
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  5. Article ; Online: Identification of ASAH1 as a susceptibility gene for familial keloids.

    Santos-Cortez, Regie Lyn P / Hu, Ying / Sun, Fanyue / Benahmed-Miniuk, Fairouz / Tao, Jian / Kanaujiya, Jitendra K / Ademola, Samuel / Fadiora, Solomon / Odesina, Victoria / Nickerson, Deborah A / Bamshad, Michael J / Olaitan, Peter B / Oluwatosin, Odunayo M / Leal, Suzanne M / Reichenberger, Ernst J

    European journal of human genetics : EJHG

    2017  Volume 25, Issue 10, Page(s) 1155–1161

    Abstract: Keloids result from abnormal proliferative scar formation with scar tissue expanding beyond the margin of the original wound and are mostly found in individuals of sub-Saharan African descent. The etiology of keloids has not been resolved but previous ... ...

    Abstract Keloids result from abnormal proliferative scar formation with scar tissue expanding beyond the margin of the original wound and are mostly found in individuals of sub-Saharan African descent. The etiology of keloids has not been resolved but previous studies suggest that keloids are a genetically heterogeneous disorder. Although possible candidate genes have been suggested by genome-wide association studies using common variants, by upregulation in keloids or their involvement in syndromes that include keloid formation, rare coding variants that contribute to susceptibility in non-syndromic keloid formation have not been previously identified. Through analysis of whole-genome data we mapped a locus to chromosome 8p23.3-p21.3 with a statistically significant maximum multipoint LOD score of 4.48. This finding was followed up using exome sequencing and led to the identification of a c.1202T>C (p.(Leu401Pro)) variant in the N-acylsphingosine amidohydrolase (ASAH1) gene that co-segregates with the keloid phenotype in a large Yoruba family. ASAH1 is an acid ceramidase known to be involved in tumor formation by controlling the ratio of ceramide and sphingosine. ASAH1 is also involved in cell proliferation and inflammation, and may affect the development of keloids via multiple mechanisms. Functional studies need to clarify the role of the ASAH1 variant in wound healing.
    MeSH term(s) Acid Ceramidase/genetics ; Adult ; Female ; Humans ; Keloid/diagnosis ; Keloid/genetics ; Male ; Mutation, Missense ; Pedigree
    Chemical Substances ASAH1 protein, human (EC 3.5.1.23) ; Acid Ceramidase (EC 3.5.1.23)
    Language English
    Publishing date 2017-07-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1141470-4
    ISSN 1476-5438 ; 1018-4813
    ISSN (online) 1476-5438
    ISSN 1018-4813
    DOI 10.1038/ejhg.2017.121
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    Zs.A 3589: Show issues Location:
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  6. Article ; Online: 2-D gel electrophoresis-based proteomic analysis reveals that ormeloxifen induces G0-G1 growth arrest and ERK-mediated apoptosis in chronic myeloid leukemia cells K562.

    Pal, Pooja / Kanaujiya, Jitendra K / Lochab, Savita / Tripathi, Shashi B / Bhatt, Madan L B / Singh, Pradhyumna K / Sanyal, Sabyasachi / Trivedi, Arun K

    Proteomics

    2011  Volume 11, Issue 8, Page(s) 1517–1529

    Abstract: Ormeloxifen is a nonsteroidal selective estrogen receptor modulator (SERM) and has been shown to possess anticancer activities in breast and uterine cancer. Here, we show that ormeloxifen induces apoptosis in dose-dependent manner in a variety of ... ...

    Abstract Ormeloxifen is a nonsteroidal selective estrogen receptor modulator (SERM) and has been shown to possess anticancer activities in breast and uterine cancer. Here, we show that ormeloxifen induces apoptosis in dose-dependent manner in a variety of leukemia cells, more strikingly in K562. 2-DE-gel electrophoresis of K562 cells induced with ormeloxifen showed that 57 and 30% of proteins belong to apoptosis and cell-cycle pathways, respectively. Our data demonstrate that ormeloxifen-induced apoptosis in K562 cells involves activation of extracellular signal-regulated kinases (ERKs) and subsequent cytochrome c release, leading to mitochondria-mediated caspase-3 activation. Ormeloxifen-induced apoptosis via ERK activation was drastically inhibited by prior treatment of K562 cells with ERK inhibitor PD98059. Ormeloxifen also inhibits proliferation of K562 cells by blocking them in G0-G1 phase by inhibiting c-myc promoter via ormeloxifen-induced MBP-1 (c-myc promoter-binding protein) and upregulation of p21 expression. We further show that ormeloxifen-induced apoptosis in K562 is translatable to mononuclear cells isolated from chronic myeloid leukemia (CML) patients. Thus, ormeloxifen induces apoptosis in K562 cells via phosphorylation of ERK and arrests them in G0-G1 phase by reciprocal regulation of p21 and c-myc. Therefore, inclusion of ormeloxifen in the therapy of chronic myeloid leukemia can be of potential utility.
    MeSH term(s) Apoptosis/drug effects ; Benzopyrans/pharmacology ; Caspase 3/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/biosynthesis ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; DNA-Binding Proteins/metabolism ; Electrophoresis, Gel, Two-Dimensional ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Flavonoids/metabolism ; Flavonoids/pharmacology ; G1 Phase/drug effects ; Humans ; In Situ Nick-End Labeling ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Mass Spectrometry ; Mitochondria/metabolism ; Phosphorylation ; Polymerase Chain Reaction ; Promoter Regions, Genetic/drug effects ; Proteomics ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Resting Phase, Cell Cycle/drug effects
    Chemical Substances Benzopyrans ; CDKN1A protein, human ; Cyclin-Dependent Kinase Inhibitor p21 ; DENND4A protein, human ; DNA-Binding Proteins ; Flavonoids ; MYC protein, human ; Proto-Oncogene Proteins c-myc ; ormeloxifene (44AXY5VE90) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Caspase 3 (EC 3.4.22.-) ; 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (SJE1IO5E3I)
    Language English
    Publishing date 2011-02-25
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2032093-0
    ISSN 1615-9861 ; 1615-9853
    ISSN (online) 1615-9861
    ISSN 1615-9853
    DOI 10.1002/pmic.201000720
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  7. Article ; Online: Proteomic identification of E6AP as a molecular target of tamoxifen in MCF7 cells.

    Lochab, Savita / Pal, Pooja / Kanaujiya, Jitendra K / Tripathi, Shashi B / Kapoor, Isha / Bhatt, Madan L B / Sanyal, Sabyasachi / Behre, Gerhard / Trivedi, Arun K

    Proteomics

    2012  Volume 12, Issue 9, Page(s) 1363–1377

    Abstract: Tamoxifen (Tam) is most widely used selective estrogen receptor modulator (SERM) for treatment of hormone-responsive breast cancer. Despite being regularly used in clinical therapy for breast cancer since 1971, the mechanism of Tam action remains largely ...

    Abstract Tamoxifen (Tam) is most widely used selective estrogen receptor modulator (SERM) for treatment of hormone-responsive breast cancer. Despite being regularly used in clinical therapy for breast cancer since 1971, the mechanism of Tam action remains largely unclear. In order to gain insights into Tam-mediated antibreast cancer actions, we applied 2DE and MS based proteomics approach to identify target proteins of Tam. We identified E6-associated protein, i.e. E6AP (UBE3A) among others to be regulated by Tam that otherwise is upregulated in breast tumors. We confirmed our 2DE finding by immunoblotting and further show that Tam leads to inhibition of E6AP expression presumably by promoting its autoubiquitination, which is coupled with nuclear export and subsequent proteasome-mediated degradation. Furthermore, we show that Tam- and siE6AP-mediated inhibition of E6AP leads to enhanced G0-G1 growth arrest and apoptosis, which is also evident from significant upregulation of cytochrome-c, Bax, p21, and PARP cleavage. Taken together, our data suggest that, Tam-targeted E6AP inhibition is in fact required for Tam-mediated antibreast cancer actions. Thus, E6AP may be a therapeutic target in breast cancer.
    MeSH term(s) Antineoplastic Agents, Hormonal/pharmacology ; Apoptosis/drug effects ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Cycle Checkpoints/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cytoplasm/metabolism ; Electrophoresis, Gel, Two-Dimensional ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; HEK293 Cells ; Humans ; Mass Spectrometry ; Molecular Targeted Therapy/methods ; Proteasome Endopeptidase Complex/metabolism ; Proteins/chemistry ; Proteins/classification ; Proteins/metabolism ; Proteome/analysis ; Proteome/drug effects ; Proteome/metabolism ; Tamoxifen/pharmacology ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Antineoplastic Agents, Hormonal ; Estrogen Receptor alpha ; Proteins ; Proteome ; Ubiquitin ; Tamoxifen (094ZI81Y45) ; UBE3A protein, human (EC 2.3.2.26) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2012-05
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2032093-0
    ISSN 1615-9861 ; 1615-9853
    ISSN (online) 1615-9861
    ISSN 1615-9853
    DOI 10.1002/pmic.201100572
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