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   Articles with "null mice" as a keyword



Neurogranin Regulates Alcohol Sensitivity through AKT Pathway in the Nucleus Accumbens

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recommendations! Published in 2019 at "PROTEOMICS"

DOI: 10.1002/pmic.201900266

Abstract: Dysfunction of glutamate neurotransmission in the nucleus accumbens (NAc) has been implicated in the pathophysiology of alcohol use disorders (AUD). Neurogranin (Ng) is exclusively expressed in the brain and mediates N‐methyl‐d‐aspartate receptor (NMDAR) hypo‐function by… read more here.

Keywords: null mice; alcohol sensitivity; nucleus accumbens; mice ... See more keywords

Inhibition of osteoclast differentiation and collagen antibody-induced arthritis by CTHRC1.

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recommendations! Published in 2017 at "Bone"

DOI: 10.1016/j.bone.2017.01.022

Abstract: Collagen triple helix repeat-containing1 (Cthrc1) has previously been implicated in osteogenic differentiation and positive regulation of bone mass, however, the underlying mechanisms remain unclear. Here we characterized the bone phenotype of a novel Cthrc1 null… read more here.

Keywords: null mice; cthrc1; bone; differentiation ... See more keywords

Dcf1 deficiency induces hypomyelination by activating Wnt signaling

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recommendations! Published in 2021 at "Experimental Neurology"

DOI: 10.1016/j.expneurol.2020.113486

Abstract: Myelination is extremely important in achieving neural function. Hypomyelination causes a variety of neurological diseases. However, little is known about how hypomyelination occurs. Here we investigated the effect of dendritic cell factor 1(Dcf1) on myelination,… read more here.

Keywords: null mice; dcf1; hypomyelination; myelination ... See more keywords

Defective GABAergic neurotransmission in the nucleus tractus solitarius in Mecp2-null mice, a model of Rett syndrome

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recommendations! Published in 2018 at "Neurobiology of Disease"

DOI: 10.1016/j.nbd.2017.09.006

Abstract: Rett syndrome (RTT) is a devastating neurodevelopmental disorder caused by loss-of-function mutations in the X-linked methyl-CpG binding protein 2 (Mecp2) gene. GABAergic dysfunction has been implicated contributing to the respiratory dysfunction, one major clinical feature… read more here.

Keywords: null mice; nucleus tractus; rett syndrome; mecp2 null ... See more keywords

Hepatic carboxylesterases are differentially regulated in PPARα-null mice treated with perfluorooctanoic acid.

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recommendations! Published in 2019 at "Toxicology"

DOI: 10.1016/j.tox.2019.01.014

Abstract: Hepatic carboxylesterases (Ces) catalyze the metabolism of drugs, environmental toxicants, and endogenous lipids and are known to be regulated by multiple nuclear receptors. Perfluorooctanoic acid (PFOA) is a synthetic fluorochemical that has been associated with… read more here.

Keywords: null mice; pfoa; hepatic carboxylesterases; mice ... See more keywords

Targeted Metabolomics Reveals a Protective Role for Basal PPARα in Cholestasis Induced by α-Naphthylisothiocyanate.

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recommendations! Published in 2018 at "Journal of proteome research"

DOI: 10.1021/acs.jproteome.7b00838

Abstract: α-Naphthylisothiocyanate (ANIT) is an experimental agent used to induce intrahepatic cholestasis. The Ppara-null mouse line is widely employed to explore the physiological and pathological roles of PPARα. However, little is known about how PPARα influences… read more here.

Keywords: null mice; ppara null; mice; basal ppar ... See more keywords

Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus

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recommendations! Published in 2017 at "Nature Communications"

DOI: 10.1038/ncomms14577

Abstract: NF-E2-related factor-2 (Nrf2) regulates cellular responses to oxidative and electrophilic stress. Loss of Keap1 increases Nrf2 protein levels, and Keap1-null mice die of oesophageal hyperkeratosis because of Nrf2 hyperactivation. Here we show that deletion of… read more here.

Keywords: null mice; hyperactivation; keap1 null; nephrogenic diabetes ... See more keywords

Slit1 inhibits ovarian follicle development and female fertility in mice

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recommendations! Published in 2024 at "Biology of Reproduction"

DOI: 10.1093/biolre/ioae106

Abstract: Abstract Previous in vitro studies have suggested that SLIT ligands could play roles in regulating ovarian granulosa cell proliferation and gene expression, as well as luteolysis. However, no in vivo study of Slit gene function… read more here.

Keywords: follicle; null mice; biology; slit1 ... See more keywords

Constitutive Epidermal Expression of Osteopontin in Osteopontin-Null Mice Restores Ultraviolet B-Induced Cutaneous Squamous Cell Carcinomas to Wild-Type Levels.

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recommendations! Published in 2025 at "Carcinogenesis"

DOI: 10.1093/carcin/bgaf034

Abstract: Studies of osteopontin (OPN)-null mice have supported the role of OPN as a critical factor in the promotion of skin tumorigenesis. OPN is a highly inducible integrin- and CD44-interacting acidic glycoprotein with pleiotropic functions. In… read more here.

Keywords: mice; null mice; constitutive epidermal; opn null ... See more keywords

A2A Receptor Contributes to Tumor Progression in P2X7 Null Mice

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recommendations! Published in 2022 at "Frontiers in Cell and Developmental Biology"

DOI: 10.1101/2022.02.28.482298

Abstract: ATP and adenosine are key constituents of the tumor niche where they exert opposite and complementary roles. ATP promotes tumor growth but also immune eradicating responses mainly via the P2X7 receptor (P2X7R), while adenosine acts… read more here.

Keywords: null mice; receptor; tumor; p2x7 null ... See more keywords

Abstract 4141690: Bisphosphonate therapy improves bone deficits but worsens arterial calcification in Mgp -null mice

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recommendations! Published in 2024 at "Circulation"

DOI: 10.1161/circ.150.suppl_1.4141690

Abstract: Background: Arterial calcification often occurs with bone mineral loss in osteoporosis, for which bisphosphonates are a standard therapy. Mice lacking the matrix GLA protein (Mgp) exhibit lethal arterial calcification and cranial bone formation deficits causing… read more here.

Keywords: mgp null; null mice; arterial calcification; calcification ... See more keywords