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Article ; Online: Cancer metabolism within tumor microenvironments.

Aki, Sho / Nakahara, Ryuichi / Maeda, Keisuke / Osawa, Tsuyoshi

Biochimica et biophysica acta. General subjects

2023 Volume 1867, Issue 5, Page(s) 130330

Abstract: Background: Tumor microenvironments could determine cancer heterogeneity and malignancy. Hypoxia, nutrition starvation, and acidic pH could contribute to cancer malignancy associated with genetic, epigenetic, and metabolic alterations, promoting ... ...

Abstract	Background: Tumor microenvironments could determine cancer heterogeneity and malignancy. Hypoxia, nutrition starvation, and acidic pH could contribute to cancer malignancy associated with genetic, epigenetic, and metabolic alterations, promoting invasion and metastasis. Cancer cells adapting to extreme tumor microenvironments could enable evasion of cell death and immune responses. It could stimulate drug resistance and recurrence, resulting in poor patient prognosis. Therefore, investigating druggable targets of the malignant cancer cells within tumor microenvironments is necessary, but such treatments are limited. Cell-cell metabolic interaction may also contribute to cancer malignancy within the tumor microenvironments. Organelle-organelle interactions have recently gained attention as new cancer therapy targets as they play essential roles in the metabolic adaptation to the tumor microenvironment. In this review, we overview (1) metabolic alterations within tumor microenvironments, (2) cell-to-cell, and (3) organelle-to-organelle metabolic interactions, and we add novel insights into cancer therapy.
MeSH term(s)	Humans ; Tumor Microenvironment ; Neoplasms/metabolism ; Cell Hypoxia ; Hypoxia
Language	English
Publishing date	2023-02-16
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2023.130330
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Article ; Online: Metabolic adaptations of cancer in extreme tumor microenvironments.

Nakahara, Ryuichi / Maeda, Keisuke / Aki, Sho / Osawa, Tsuyoshi

Cancer science

2023 Volume 114, Issue 4, Page(s) 1200–1207

Abstract: Cancer cells are highly heterogeneous to adapt to extreme tumor microenvironments (TMEs). TMEs challenge cancer cells via hypoxia, nutrition starvation, and acidic pH, promoting invasion and metastasis concomitant with genetic, epigenetic, and metabolic ... ...

Abstract	Cancer cells are highly heterogeneous to adapt to extreme tumor microenvironments (TMEs). TMEs challenge cancer cells via hypoxia, nutrition starvation, and acidic pH, promoting invasion and metastasis concomitant with genetic, epigenetic, and metabolic alterations. Metabolic adaptation to an extreme TME could allow cancer cells to evade cell death and immune responses, as well as resulting in drug resistance, recurrence, and poor patient prognosis. Therefore, elucidation of the metabolic adaptation of malignant cancer cells within TMEs is necessary, however, most are still elusive. Recently, adaptation of cancer cells within the TME can be analyzed via cell-cell interactions at the single-cell level. In addition, information into organelle-organelle interactions has recently been obtained. These cell-cell, and organelle-organelle interactions demonstrate the potential as new cancer therapy targets, as they play essential roles in the metabolic adaptation of cancer cells to the TME. In this manuscript, we review (1) metabolic adaptations within tumor microenvironments through (2) cell-to-cell, and (3) organelle-organelle metabolic interactions.
MeSH term(s)	Humans ; Tumor Microenvironment ; Neoplasms/pathology ; Energy Metabolism ; Cell Communication ; Hypoxia
Language	English
Publishing date	2023-01-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1349-7006
ISSN (online)	1349-7006
ISSN	1349-7006
DOI	10.1111/cas.15722
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Article ; Online: Class II phosphatidylinositol 3-kinase-C2α is essential for Notch signaling by regulating the endocytosis of γ-secretase in endothelial cells.

Shimizu, Shota / Yoshioka, Kazuaki / Aki, Sho / Takuwa, Yoh

Scientific reports

2021 Volume 11, Issue 1, Page(s) 5199

Abstract: The class II α-isoform of phosphatidylinositol 3-kinase (PI3K-C2α) plays a crucial role in angiogenesis at least in part through participating in endocytosis and, thereby, endosomal signaling of several cell surface receptors including VEGF receptor-2 ... ...

Abstract	The class II α-isoform of phosphatidylinositol 3-kinase (PI3K-C2α) plays a crucial role in angiogenesis at least in part through participating in endocytosis and, thereby, endosomal signaling of several cell surface receptors including VEGF receptor-2 and TGFβ receptor in vascular endothelial cells (ECs). The Notch signaling cascade regulates many cellular processes including cell proliferation, cell fate specification and differentiation. In the present study, we explored a role of PI3K-C2α in Delta-like 4 (Dll4)-induced Notch signaling in ECs. We found that knockdown of PI3K-C2α inhibited Dll4-induced generation of the signaling molecule Notch intracellular domain 1 (NICD1) and the expression of Notch1 target genes including HEY1, HEY2 and NOTCH3 in ECs but not in vascular smooth muscle cells. PI3K-C2α knockdown did not inhibit Dll4-induced endocytosis of cell surface Notch1. In contrast, PI3K-C2α knockdown as well as clathrin heavy chain knockdown impaired endocytosis of Notch1-cleaving protease, γ-secretase complex, with the accumulation of Notch1 at the perinuclear endolysosomes. Pharmacological blockage of γ-secretase also induced the intracellular accumulation of Notch1. Taken together, we conclude that PI3K-C2α is required for the clathrin-mediated endocytosis of γ-secretase complex, which allows for the cleavage of endocytosed Notch1 by γ-secretase complex at the endolysosomes to generate NICD1 in ECs.
MeSH term(s)	Amyloid Precursor Protein Secretases/genetics ; Amyloid Precursor Protein Secretases/metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Clathrin/genetics ; Endocytosis/genetics ; Endothelial Cells/metabolism ; Human Umbilical Vein Endothelial Cells ; Humans ; Neovascularization, Physiologic/genetics ; Neovascularization, Physiologic/physiology ; Phosphatidylinositol 3-Kinases/genetics ; Receptor, Notch1/genetics ; Receptor, Notch3/genetics ; Receptor, Transforming Growth Factor-beta Type I/genetics ; Repressor Proteins/genetics ; Signal Transduction/genetics ; Vascular Endothelial Growth Factor Receptor-2/genetics
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Clathrin ; HEY2 protein, human ; Hairy, HRT1 protein ; Receptor, Notch1 ; Receptor, Notch3 ; Repressor Proteins ; PIK3C2A protein, human (EC 2.7.1.137) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; TGFBR1 protein, human (EC 2.7.11.30) ; Amyloid Precursor Protein Secretases (EC 3.4.-)
Language	English
Publishing date	2021-03-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-84548-4
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Article ; Online: TGFβ receptor endocytosis and Smad signaling require synaptojanin1, PI3K-C2α-, and INPP4B-mediated phosphoinositide conversions.

Aki, Sho / Yoshioka, Kazuaki / Takuwa, Noriko / Takuwa, Yoh

Molecular biology of the cell

2020 Volume 31, Issue 5, Page(s) 360–372

Abstract: Phosphoinositide conversion regulates a diverse array of dynamic membrane events including endocytosis. However, it is not well understood which enzymes are involved in phosphoinositide conversions for receptor endocytosis. We found by small interfering ... ...

Abstract	Phosphoinositide conversion regulates a diverse array of dynamic membrane events including endocytosis. However, it is not well understood which enzymes are involved in phosphoinositide conversions for receptor endocytosis. We found by small interfering RNA (siRNA)-mediated knockdown (KD) that class II PI3K α-isoform (PI3K-C2α), the 5'-phosphatase synaptojanin1 (Synj1), and the 4'-phosphatase INPP4B, but not PI3K-C2β, Synj2, or INPP4A, were required for TGFβ-induced endocytosis of TGFβ receptor. TGFβ induced rapid decreases in PI(4,5)P
MeSH term(s)	Activin Receptors, Type II/metabolism ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Endocytosis ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Nerve Tissue Proteins/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositols/metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Phosphorylation ; Receptor, Transforming Growth Factor-beta Type I/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction ; Smad Proteins/metabolism ; Transforming Growth Factor beta/metabolism
Chemical Substances	Nerve Tissue Proteins ; Phosphatidylinositols ; Receptors, Transforming Growth Factor beta ; Smad Proteins ; Transforming Growth Factor beta ; ACVRL1 protein, human (EC 2.7.11.30) ; Activin Receptors, Type II (EC 2.7.11.30) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; TGFBR1 protein, human (EC 2.7.11.30) ; synaptojanin (EC 3.1.3.-) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; phosphatidylinositol-3,4-bisphosphate 4-phosphatase (EC 3.1.3.66)
Language	English
Publishing date	2020-01-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1098979-1
ISSN	1939-4586 ; 1059-1524
ISSN (online)	1939-4586
ISSN	1059-1524
DOI	10.1091/mbc.E19-11-0662
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Zs.A 2853: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Early Phase Enamel Bond Performance of a Two-step Adhesive Containing a Primer Derived from a Universal Adhesive.

Iwase, Kei / Takamizawa, Toshiki / Sai, Keiichi / Shibas Aki, Sho / Barkmeier, Wayne W / Latta, Mark A / Kamimoto, Atsushi / Miyazaki, Masashi

The journal of adhesive dentistry

2022 Volume 24, Issue 1, Page(s) 407–420

Abstract: Purpose: To investigate the changes in the enamel bond performance of a two-step adhesive containing a primer derived from a universal adhesive in the early phase before 24 h and compare them to those of other adhesives. The Knoop hardness number (KHN) ... ...

Abstract	Purpose: To investigate the changes in the enamel bond performance of a two-step adhesive containing a primer derived from a universal adhesive in the early phase before 24 h and compare them to those of other adhesives. The Knoop hardness number (KHN) of the cured adhesive layers and resin composite was measured. Materials and methods: A new two-step adhesive using universal adhesive technology, G2-Bond Universal, was tested. Two conventional two-step adhesives, Clearfil SE Bond 2 and OptiBond eXTRa, and an established universal adhesive, Scotchbond Universal Plus Adhesive, were used as comparison materials. Twelve specimens per group were used to measure the shear bond strength (SBS) to bovine enamel in different etching modes. The bonded specimens were stored in distilled water at 37°C for 5 min or 1, 6, 12, or 24 h before SBS testing. The KHN of the adhesive layer and resin composite was determined after the same storage periods as for SBS testing. Results: All adhesives exhibited increased SBS with prolonged storage periods, irrespective of the etching mode. The KHN of the adhesive layer and resin composite increased over time. Conclusions: There were strong positive correlations between the SBS and KHN of the adhesive layer and resin composite. Phosphoric acid pre-etching of enamel effectively increases enamel bond performance. The two-step adhesive G2-Bond Universal demonstrated significantly higher bond strength in the early phase than the other adhesives in self-etch mode.
MeSH term(s)	Cattle ; Animals ; Acid Etching, Dental ; Dentin-Bonding Agents/chemistry ; Dental Bonding ; Dental Cements/chemistry ; Materials Testing ; Resin Cements/chemistry ; Dental Enamel/chemistry ; Shear Strength ; Composite Resins
Chemical Substances	Dentin-Bonding Agents ; Dental Cements ; Resin Cements ; Composite Resins
Language	English
Publishing date	2022-11-08
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2002396-0
ISSN	1757-9988 ; 1461-5185
ISSN (online)	1757-9988
ISSN	1461-5185
DOI	10.3290/j.jad.b3559035
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Article ; Online: Class II phosphatidylinositol 3-kinase α and β isoforms are required for vascular smooth muscle Rho activation, contraction and blood pressure regulation in mice.

Islam, Shahidul / Yoshioka, Kazuaki / Aki, Sho / Ishimaru, Kazuhiro / Yamada, Hiroki / Takuwa, Noriko / Takuwa, Yoh

The journal of physiological sciences : JPS

2020 Volume 70, Issue 1, Page(s) 18

Abstract: Class II phosphatidylinositol 3-kinases (PI3K), PI3K-C2α and PI3K-C2β, are involved in cellular processes including endocytosis, cilia formation and autophagy. However, the role of PI3K-C2α and PI3K-C2β at the organismal level is not well understood. We ... ...

Abstract	Class II phosphatidylinositol 3-kinases (PI3K), PI3K-C2α and PI3K-C2β, are involved in cellular processes including endocytosis, cilia formation and autophagy. However, the role of PI3K-C2α and PI3K-C2β at the organismal level is not well understood. We found that double knockout (KO) mice with both smooth muscle-specific KO of PI3K-C2α and global PI3K-C2β KO, but not single KO mice of either PI3K-C2α or PI3K-C2β, exhibited reductions in arterial blood pressure and substantial attenuation of contractile responses of isolated aortic rings. In wild-type vascular smooth muscle cells, double knockdown of PI3K-C2α and PI3K-C2β but not single knockdown of either PI3K markedly inhibited contraction with reduced phosphorylation of 20-kDa myosin light chain and MYPT1 and Rho activation, but without inhibition of the intracellular Ca
MeSH term(s)	Animals ; Blood Pressure/physiology ; Calcium/metabolism ; Cells, Cultured ; Class II Phosphatidylinositol 3-Kinases/genetics ; Class II Phosphatidylinositol 3-Kinases/metabolism ; Disease Models, Animal ; Isoenzymes ; Mice ; Mice, Knockout ; Muscle Contraction/physiology ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/physiology ; rho GTP-Binding Proteins/genetics ; rho GTP-Binding Proteins/metabolism
Chemical Substances	Isoenzymes ; Class II Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; rho GTP-Binding Proteins (EC 3.6.5.2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-03-19
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2234472-X
ISSN	1880-6562 ; 1880-6546
ISSN (online)	1880-6562
ISSN	1880-6546
DOI	10.1186/s12576-020-00745-2
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Article ; Online: Acidic extracellular pH drives accumulation of N1-acetylspermidine and recruitment of protumor neutrophils.

Kato, Miki / Maeda, Keisuke / Nakahara, Ryuichi / Hirose, Haruka / Kondo, Ayano / Aki, Sho / Sugaya, Maki / Hibino, Sana / Nishida, Miyuki / Hasegawa, Manami / Morita, Hinano / Ando, Ritsuko / Tsuchida, Rika / Yoshida, Minoru / Kodama, Tatsuhiko / Yanai, Hideyuki / Shimamura, Teppei / Osawa, Tsuyoshi

PNAS nexus

2023 Volume 2, Issue 10, Page(s) pgad306

Abstract: An acidic tumor microenvironment plays a critical role in tumor progression. However, understanding of metabolic reprogramming of tumors in response to acidic extracellular pH has remained elusive. Using comprehensive metabolomic analyses, we ... ...

Abstract	An acidic tumor microenvironment plays a critical role in tumor progression. However, understanding of metabolic reprogramming of tumors in response to acidic extracellular pH has remained elusive. Using comprehensive metabolomic analyses, we demonstrated that acidic extracellular pH (pH 6.8) leads to the accumulation of N1-acetylspermidine, a protumor metabolite, through up-regulation of the expression of spermidine/spermine acetyltransferase 1 (
Language	English
Publishing date	2023-10-10
Publishing country	England
Document type	Journal Article
ISSN	2752-6542
ISSN (online)	2752-6542
DOI	10.1093/pnasnexus/pgad306
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Article ; Online: The class II phosphoinositide 3-kinases PI3K-C2α and PI3K-C2β differentially regulate clathrin-dependent pinocytosis in human vascular endothelial cells.

Aung, Khin Thuzar / Yoshioka, Kazuaki / Aki, Sho / Ishimaru, Kazuhiro / Takuwa, Noriko / Takuwa, Yoh

The journal of physiological sciences : JPS

2018 Volume 69, Issue 2, Page(s) 263–280

Abstract: Pinocytosis is an important fundamental cellular process that is used by the cell to transport fluid and solutes. Phosphoinositide 3-kinases (PI3Ks) regulate a diverse array of dynamic membrane events. However, it is not well-understood which PI3K ... ...

Abstract	Pinocytosis is an important fundamental cellular process that is used by the cell to transport fluid and solutes. Phosphoinositide 3-kinases (PI3Ks) regulate a diverse array of dynamic membrane events. However, it is not well-understood which PI3K isoforms are involved in specific mechanisms of pinocytosis. We performed knockdown studies of endogenous PI3K isoforms and clathrin heavy chain (CHC) mediated by small interfering RNA (siRNA). The results demonstrated that the class II PI3K PI3K-C2α and PI3K-C2β, but not the class I or III PI3K, were required for pinocytosis, based on an evaluation of fluorescein-5-isothiocyanate (FITC)-dextran uptake in endothelial cells. Pinocytosis was partially dependent on both clathrin and dynamin, and both PI3K-C2α and PI3K-C2β were required for clathrin-mediated-but not clathrin-non-mediated-FITC-dextran uptake at the step leading up to its delivery to early endosomes. Both PI3K-C2α and PI3K-C2β were co-localized with clathrin-coated pits and vesicles. However, PI3K-C2β, but not PI3K-C2α, was highly co-localized with actin filament-associated clathrin-coated structures and required for actin filament formation at the clathrin-coated structures. These results indicate that PI3K-C2α and PI3K-C2β play differential, indispensable roles in clathrin-mediated pinocytosis.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Animals ; Cells, Cultured ; Class II Phosphatidylinositol 3-Kinases/metabolism ; Clathrin/metabolism ; Endothelial Cells/metabolism ; Endothelial Cells/physiology ; Human Umbilical Vein Endothelial Cells ; Humans ; Phosphatidylinositol 3-Kinases/metabolism ; Pinocytosis/physiology ; RNA, Small Interfering/metabolism
Chemical Substances	Clathrin ; RNA, Small Interfering ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Class II Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3C2A protein, human (EC 2.7.1.137) ; PIK3C2B protein, human (EC 2.7.1.137)
Language	English
Publishing date	2018-10-29
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2234472-X
ISSN	1880-6562 ; 1880-6546
ISSN (online)	1880-6562
ISSN	1880-6546
DOI	10.1007/s12576-018-0644-2
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Article ; Online: Pathological complete remission of relapsed tumor by photo-activating antibody-mimetic drug conjugate treatment.

Kaneko, Yudai / Yamatsugu, Kenzo / Yamashita, Takefumi / Takahashi, Kazuki / Tanaka, Toshiya / Aki, Sho / Tatsumi, Toshifumi / Kawamura, Takeshi / Miura, Mai / Ishii, Masazumi / Ohkubo, Kei / Osawa, Tsuyoshi / Kodama, Tatsuhiko / Ishikawa, Shumpei / Tsukagoshi, Masanobu / Chansler, Michael / Sugiyama, Akira / Kanai, Motomu / Katoh, Hiroto

Cancer science

2022

Abstract: Antibody-mimetic drug conjugate is a novel noncovalent conjugate consisting of an antibody-mimetic recognizing a target molecule on the cancer cell surface and low-molecular-weight payloads that kill the cancer cells. In this study, the efficacy of a ... ...

Abstract	Antibody-mimetic drug conjugate is a novel noncovalent conjugate consisting of an antibody-mimetic recognizing a target molecule on the cancer cell surface and low-molecular-weight payloads that kill the cancer cells. In this study, the efficacy of a photo-activating antibody-mimetic drug conjugate targeting HER2-expressing tumors was evaluated in mice, by using the affibody that recognize HER2 (Z
Language	English
Publishing date	2022-09-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1349-7006
ISSN (online)	1349-7006
ISSN	1349-7006
DOI	10.1111/cas.15565
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Article ; Online: Antibody mimetic drug conjugate manufactured by high-yield Escherichia coli expression and non-covalent binding system.

Yamatsugu, Kenzo / Katoh, Hiroto / Yamashita, Takefumi / Takahashi, Kazuki / Aki, Sho / Tatsumi, Toshifumi / Kaneko, Yudai / Kawamura, Takeshi / Miura, Mai / Ishii, Masazumi / Ohkubo, Kei / Osawa, Tsuyoshi / Kodama, Tatsuhiko / Ishikawa, Shumpei / Kanai, Motomu / Sugiyama, Akira

Protein expression and purification

2021 Volume 192, Page(s) 106043

Abstract: Antibody-drug conjugates (ADCs) are a major therapeutic tool for the treatment of advanced cancer. Malignant cells in advanced cancer often display multiple genetic mutations and become resistant to monotherapy. Therefore, a therapeutic regimen that ... ...

Abstract	Antibody-drug conjugates (ADCs) are a major therapeutic tool for the treatment of advanced cancer. Malignant cells in advanced cancer often display multiple genetic mutations and become resistant to monotherapy. Therefore, a therapeutic regimen that simultaneously targets multiple molecules with multiple payloads is desirable. However, the development of ADCs is hampered by issues in biopharmaceutical manufacturing and the complexity of the conjugation process of low-molecular-weight payloads to biologicals. Here, we report antibody mimetic-drug conjugates (AMDCs) developed by exploiting the non-covalent binding property of payloads based on high-affinity binding of mutated streptavidin and modified iminobiotin. Miniprotein antibodies were fused to a low immunogenic streptavidin variant, which was then expressed in Escherichia coli inclusion bodies, solubilized, and refolded into functional tetramers. The AMDC developed against human epidermal growth factor receptor 2 (HER2) effectively killed cultured cancer cells using bis-iminobiotin conjugated to photo-activating silicon phthalocyanine. The HER2-targeting AMDC was also effective in vivo against a mouse KPL-4 xenograft model. This AMDC platform provides rapid, stable, and high-yield therapeutics against multiple targets.
MeSH term(s)	Animals ; Biotin/administration & dosage ; Biotin/analogs & derivatives ; Biotin/chemistry ; Biotin/genetics ; Biotin/immunology ; Cell Line, Tumor ; Cloning, Molecular ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Gene Expression ; Humans ; Immunoconjugates/administration & dosage ; Immunoconjugates/chemistry ; Immunoconjugates/genetics ; Immunoconjugates/immunology ; Mice ; Mice, Inbred BALB C ; Neoplasms/drug therapy ; Protein Folding ; Receptor, ErbB-2/antagonists & inhibitors ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/immunology ; Streptavidin/administration & dosage ; Streptavidin/chemistry ; Streptavidin/genetics ; Streptavidin/immunology
Chemical Substances	Immunoconjugates ; iminobiotin ; Biotin (6SO6U10H04) ; Streptavidin (9013-20-1) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2021-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1055455-5
ISSN	1096-0279 ; 1046-5928
ISSN (online)	1096-0279
ISSN	1046-5928
DOI	10.1016/j.pep.2021.106043
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