B6(C3H)-Crhm1H/H

Status

Available to order

EMMA IDEM:09024
Citation informationRRID:IMSR_EM:09024 

Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information.

 
International strain nameB6(C3H)-Crhm1H/H
Alternative nameTreacle-B6
Strain typeInduced Mutant Strains : Chemically-induced
Allele/Transgene symbolCrhm1H
Gene/Transgene symbolCrh

Information from provider

ProviderRoger Cox
Provider affiliationMRC Harwell
Genetic informationA point mutation at -120bp of the promoter region of the Crh gene.
Phenotypic informationHomozygous:
Not able to produce homozygotes.

Heterozygous:
Heterozygous Crh mice are obese, exhibit muscle wasting, thin skin, hair loss, elevated plasma and urinary corticosterone, hyperglycaemia, hyperinsulinaemia, hypercholesterolemia, hypertriglyceridemia and hyperleptinaemia. They also have low bone mineral density, hypercalcemia, hypercalciuria and decreased concentrations of plasma parathyroid hormone and osteocalcin.
Breeding historyOriginal mutant (CBMLC/329.5b) was the offspring of a C57BL/6J male that received ENU, mated to a C3H/HeH female. The causative mutation is a point mutation at -120bp of the promoter region of the Crh gene. The material that has been frozen down was generated by backcrossing the original mutant to C3H/HeH for 6 generations, then backcrossing to C57BL/6J for more than 10 generations.
References
  • An N-ethyl-N-nitrosourea induced corticotropin-releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excess.;Bentley Liz, Esapa Christopher T, Nesbit M Andrew, Head Rosie A, Evans Holly, Lath Darren, Scudamore Cheryl L, Hough Tertius A, Podrini Christine, Hannan Fadil M, Fraser William D, Croucher Peter I, Brown Matthew A, Brown Steve D M, Cox Roger D, Thakker Rajesh V, ;2014;Endocrinology;155;908-22; 24302625
Homozygous fertilenot known
Homozygous viablenot known
Homozygous matings requiredno
Immunocompromisednot known

Information from EMMA

Archiving centreMary Lyon Centre at MRC Harwell, Oxford, United Kingdom

Disease and phenotype information

MGI allele-associated human disease models

Orphanet associated rare diseases, based on orthologous gene matching

MGI phenotypes (allele matching)
  • decreased bone mineral density / MGI
  • increased circulating calcium level / MGI
  • thin tail / MGI
  • abnormal hepatocyte morphology / MGI
  • thin skin / MGI
  • increased body weight / MGI
  • obese / MGI
  • decreased body weight / MGI
  • polydipsia / MGI
  • increased circulating triglyceride level / MGI
  • hyperglycemia / MGI
  • increased circulating corticosterone level / MGI
  • increased urine glucose level / MGI
  • polyuria / MGI
  • abnormal homeostasis / MGI
  • abnormal glucose homeostasis / MGI
  • increased circulating insulin level / MGI
  • abnormal bone marrow morphology / MGI
  • increased circulating glucagon level / MGI
  • decreased circulating parathyroid hormone level / MGI
  • increased circulating alanine transaminase level / MGI
  • increased urine protein level / MGI
  • increased circulating alkaline phosphatase level / MGI
  • decreased lean body mass / MGI
  • abnormal corticosterone level / MGI
  • decreased osteoblast cell number / MGI
  • premature hair loss / MGI
  • increased circulating cholesterol level / MGI
  • impaired glucose tolerance / MGI
  • insulin resistance / MGI
  • increased circulating aspartate transaminase level / MGI
  • homeostasis/metabolism phenotype / MGI
  • increased urine calcium level / MGI
  • increased circulating creatinine level / MGI
  • increased circulating total protein level / MGI
  • increased circulating leptin level / MGI
  • abnormal adrenal gland zona fasciculata morphology / MGI
  • increased blood uric acid level / MGI
  • abnormal fat cell morphology / MGI
  • abnormal blood homeostasis / MGI
  • abnormal urine homeostasis / MGI
  • increased total body fat amount / MGI
  • increased urine corticosterone level / MGI
  • abnormal circulating osteocalcin level / MGI
  • increased adrenal gland weight / MGI
  • decreased bone ossification / MGI
  • decreased bone mineralization / MGI
MGI phenotypes (gene matching)
  • decreased bone mineral density / MGI
  • abnormal circulating glucose level / MGI
  • increased circulating calcium level / MGI
  • thin tail / MGI
  • abnormal hepatocyte morphology / MGI
  • abnormal adrenal gland morphology / MGI
  • abnormal lung morphology / MGI
  • abnormal lung development / MGI
  • thick pulmonary interalveolar septum / MGI
  • thin skin / MGI
  • abnormal epidermis stratum granulosum morphology / MGI
  • abnormal epidermis stratum corneum morphology / MGI
  • abnormal body weight / MGI
  • increased body weight / MGI
  • obese / MGI
  • decreased body weight / MGI
  • polydipsia / MGI
  • increased circulating triglyceride level / MGI
  • hyperglycemia / MGI
  • abnormal adrenal gland secretion / MGI
  • increased circulating corticosterone level / MGI
  • increased urine glucose level / MGI
  • polyuria / MGI
  • abnormal homeostasis / MGI
  • abnormal inflammatory response / MGI
  • decreased inflammatory response / MGI
  • abnormal glucose homeostasis / MGI
  • increased circulating insulin level / MGI
  • abnormal respiratory system physiology / MGI
  • no abnormal phenotype detected / MGI
  • abnormal bone marrow morphology / MGI
  • abnormal cell-mediated immunity / MGI
  • abnormal professional antigen presenting cell physiology / MGI
  • decreased circulating corticosterone level / MGI
  • increased circulating glucagon level / MGI
  • decreased circulating parathyroid hormone level / MGI
  • increased circulating alanine transaminase level / MGI
  • increased urine protein level / MGI
  • increased circulating alkaline phosphatase level / MGI
  • abnormal cytokine secretion / MGI
  • no phenotypic analysis / MGI
  • nervous system phenotype / MGI
  • maternal effect / MGI
  • decreased lean body mass / MGI
  • abnormal corticosterone level / MGI
  • abnormal adrenocorticotropin level / MGI
  • abnormal surfactant composition / MGI
  • decreased susceptibility to experimental autoimmune encephalomyelitis / MGI
  • decreased osteoblast cell number / MGI
  • decreased T cell proliferation / MGI
  • premature hair loss / MGI
  • increased circulating cholesterol level / MGI
  • impaired glucose tolerance / MGI
  • insulin resistance / MGI
  • increased circulating aspartate transaminase level / MGI
  • abnormal circulating corticosterone level / MGI
  • homeostasis/metabolism phenotype / MGI
  • abnormal circulating hormone level / MGI
  • increased urine calcium level / MGI
  • abnormal food intake / MGI
  • increased circulating creatinine level / MGI
  • increased circulating total protein level / MGI
  • abnormal circulating adrenaline level / MGI
  • decreased circulating adrenaline level / MGI
  • abnormal circulating noradrenaline level / MGI
  • decreased circulating leptin level / MGI
  • increased circulating leptin level / MGI
  • abnormal adrenal gland zona fasciculata morphology / MGI
  • increased circulating interleukin-6 level / MGI
  • increased blood uric acid level / MGI
  • abnormal fat cell morphology / MGI
  • increased splenocyte number / MGI
  • abnormal blood homeostasis / MGI
  • abnormal urine homeostasis / MGI
  • increased total body fat amount / MGI
  • abnormal Clara cell morphology / MGI
  • abnormal solitary pulmonary neuroendocrine cell morphology / MGI
  • increased mesenchymal cell proliferation involved in lung development / MGI
  • increased urine corticosterone level / MGI
  • abnormal circulating osteocalcin level / MGI
  • increased adrenal gland weight / MGI
  • adrenal gland atrophy / MGI
  • decreased bone ossification / MGI
  • decreased bone mineralization / MGI

Literature references

  • An N-ethyl-N-nitrosourea induced corticotropin-releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excess.;Bentley Liz, Esapa Christopher T, Nesbit M Andrew, Head Rosie A, Evans Holly, Lath Darren, Scudamore Cheryl L, Hough Tertius A, Podrini Christine, Hannan Fadil M, Fraser William D, Croucher Peter I, Brown Matthew A, Brown Steve D M, Cox Roger D, Thakker Rajesh V, ;2014;Endocrinology;155;908-22; 24302625

Information on how we integrate external resources can be found here

Order

Availabilities

Requesting frozen sperm or embryos is generally advisable wherever possible, in order to minimise the shipment of live mice.

  • Frozen sperm. Delivered in 4 weeks (after paperwork in place). €1740*
  • Rederivation of mice from frozen stock, delivery time available upon request . €3880*
  • Tissue - Types of tissue, service fee and delivery time available upon request

Due to the dynamic nature of our processes strain availability may change at short notice. The local repository manager will advise you in these circumstances.

* In addition users have to cover all the shipping costs (including the cost for returning dry-shippers, where applicable).

More details on pricing and delivery times

Practical information

Example health report
(Current health report will be provided later)

Material Transfer Agreement (MTA)
MTA will be issued after an order has been submitted.

EMMA conditions
Legally binding conditions for the transfer

Other EMMA strains

Not found what you were looking for? Search here for other strains available from EMMA.


Search
INFRAFRONTIER® and European Mouse Mutant Archive - EMMA® are registered trademarks at the European Union Intellectual Property Office (EUIPO).