Homozygous deletion of the CRABPI gene in AB1 embryonic stem cells results in increased CRABPII gene expression and decreased intracellular retinoic acid concentration (Q40665868)

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scientific article published on March 2003

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English	Homozygous deletion of the CRABPI gene in AB1 embryonic stem cells results in increased CRABPII gene expression and decreased intracellular retinoic acid concentration	scientific article published on March 2003

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scholarly article

1 reference

Europe PubMed Central

22 September 2017

Homozygous deletion of the CRABPI gene in AB1 embryonic stem cells results in increased CRABPII gene expression and decreased intracellular retinoic acid concentration (English)

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Europe PubMed Central

22 September 2017

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based on heuristic

inferred from title

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based on heuristic

inferred from title

Michelle A. Lane

3

object named as

Michelle A Lane

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Europe PubMed Central

22 September 2017

author name string

Anne C Chen

1

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Europe PubMed Central

22 September 2017

Ker Yu

2

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Europe PubMed Central

22 September 2017

Lorraine J Gudas

4

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Europe PubMed Central

22 September 2017

language of work or name

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publication date

1 March 2003

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Europe PubMed Central

22 September 2017

Archives of Biochemistry and Biophysics

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Europe PubMed Central

22 September 2017

411

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Europe PubMed Central

22 September 2017

159-173

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Europe PubMed Central

22 September 2017

2

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Europe PubMed Central

22 September 2017

Retinoids and vertebrate limb pattern formation

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9-Cis retinoic acid stereoisomer binds and activates the nuclear receptor RXRα

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RXR beta: a coregulator that enhances binding of retinoic acid, thyroid hormone, and vitamin D receptors to their cognate response elements

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All-trans and 9-cis retinoic acid induction of CRABPII transcription is mediated by RAR-RXR heterodimers bound to DR1 and DR2 repeated motifs.

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Coregulator codes of transcriptional regulation by nuclear receptors

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Molecular cloning of cDNA encoding a second cellular retinoic acid-binding protein

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Arginine 132 of cellular retinoic acid-binding protein (type II) is important for binding of retinoic acid

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The CRABP I gene contains two separable, redundant regulatory regions active in neural tissues in transgenic mouse embryos.

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Regulation of the CRABP-I gene during mouse embryogenesis.

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Differential expression of genes encoding α, β and γ retinoic acid receptors and CRABP in the developing limbs of the mouse

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Domains of cellular retinoic acid-binding protein I (CRABP I) expression in the hindbrain and neural crest of the mouse embryo

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Localization of CRABP-I and CRABP-II mRNA in the early mouse embryo by whole-mount in situ hybridization: implications for teratogenesis and neural development.

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Anteriorization of CRABP-I expression by retinoic acid in the developing mouse central nervous system and its relationship to teratogenesis.

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The roles of retinoids in vertebrate development

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Overexpression of the cellular retinoic acid binding protein-I (CRABP-I) results in a reduction in differentiation-specific gene expression in F9 teratocarcinoma cells

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Nuclear Detection of Cellular Retinoic Acid Binding Proteins I and II with New Antibodies

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Physical and functional interactions between cellular retinoic acid binding protein II and the retinoic acid-dependent nuclear complex.

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Localization of the RAR interaction domain of cellular retinoic acid binding protein-II.

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Distinct roles for cellular retinoic acid-binding proteins I and II in regulating signaling by retinoic acid

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Nuclear import of cellular retinoic acid-binding protein type I in mouse embryonic cells

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Direct channeling of retinoic acid between cellular retinoic acid-binding protein II and retinoic acid receptor sensitizes mammary carcinoma cells to retinoic acid-induced growth arrest

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The cellular retinoic acid binding protein I is dispensable.

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Normal development, growth and reproduction in cellular retinoic acid binding protein-I (CRABPI) null mutant mice

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The cellular retinoic acid binding proteins.

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10.1016/S0003-9861(02)00732-4

1 reference

Europe PubMed Central

22 September 2017

1 reference

Europe PubMed Central

22 September 2017

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