ArticleProceedings of the National Academy of Sciences of the United States of America2004
Development of hydrocephalus in mice lacking SOCS7.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- JAK-STAT signaling: molecular mechanism and targeted treatment in dento-maxillofacial abnormalities.International journal of oral science · 2026Review
- Testis-enrichedAmerican journal of translational research · 2025Article
- Genetic and molecular mechanisms of hydrocephalus.Frontiers in molecular neuroscience · 2024Review
- Review
- Identification of mutations in porcineFrontiers in veterinary science · 2022Article
- SOCS Proteins in Immunity, Inflammatory Diseases, and Immune-Related Cancer.Frontiers in medicine · 2021Review
- Genes causing congenital hydrocephalus: Their chromosomal characteristics of telomere proximity and DNA compositions.Experimental neurology · 2021Review
- Molecular Mechanisms and Risk Factors for the Pathogenesis of Hydrocephalus.Frontiers in genetics · 2021Review
- Article
- The role of small adaptor proteins in the control of oncogenic signalingr driven by tyrosine kinases in human cancer.Oncotarget · 2016Review
- Camk2a-Cre-mediated conditional deletion of chromatin remodeler Brg1 causes perinatal hydrocephalus.Neuroscience letters · 2015Article
- Cell regulation by phosphotyrosine-targeted ubiquitin ligases.Molecular and cellular biology · 2015Review
- Interferons, signal transduction pathways, and the central nervous system.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- The role of suppressors of cytokine signalling in human neoplasms.Molecular biology international · 2014Review
- Rbx2 regulates neuronal migration through different cullin 5-RING ligase adaptors.Developmental cell · 2013Article
- Disruption of the mouse Jhy gene causes abnormal ciliary microtubule patterning and juvenile hydrocephalus.Developmental biology · 2013Article
- Polymorphisms in the SOCS7 gene and glucose homeostasis traits.BMC research notes · 2013Article
- Genetic deletion of Rnd3 results in aqueductal stenosis leading to hydrocephalus through up-regulation of Notch signaling.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- SOCS proteins in infectious diseases of mammals.Veterinary immunology and immunopathology · 2013Review
- SOCS proteins in development and disease.American journal of clinical and experimental immunology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SOCS7 is a member of the suppressor of cytokine signaling (SOCS) family of proteins (SOCS1-SOCS7 and CIS). SOCS proteins are composed of an N-terminal domain of variable length, a central Src homology 2 domain, and a C-terminal SOCS box. Biochemical and genetic studies have revealed that SOCS1, SOCS2, SOCS3, and CIS play an important role in the termination of cytokine and growth factor signaling. However, the biological actions of other SOCS proteins are less well defined. To investigate the physiological role of SOCS7, we have used gene targeting to generate mice that lack expression of the Socs7 gene. Socs7-/- mice were born in expected numbers, were fertile, and did not exhibit defects in hematopoiesis or circulating glucose or insulin concentrations. However, Socs7-/- mice were 7-10% smaller than their wild-type littermates, and within 15 weeks of age approximately 50% of the Socs7-/- mice died as a result of hydrocephalus that was characterized by cranial distortion, dilation of the ventricular system, reduced thickness of the cerebral cortex, and disorganization of the subcommissural organ. In situ hybridization studies revealed prominent expression of Socs7 in the brain, suggestive of an important functional role of SOCS7 in this organ.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.