B6(C3H)-Crhm1H/H

Status

Available to order

EMMA IDEM:09024
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

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

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*

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

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