Search Criteria: Research Area is "Hematological Research: Platelet Defects"
Strains from the Research Colonies of Jackson Laboratory Scientists
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000629 | C57BL/6J-Lystbg-J/J | Level 4 |
| Mice homozygous for the beige-J spontaneous mutation (Lystbg-J) are identical to the original beige mutation (Lystbg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn
..... For more information please see the full descriiption on the strain data sheet | ||
| 007937 | B6.129-Tyro3tm1Grl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of brain lysate. Homozygotes exhibit decreased sensitivity to induced pathological thrombosis resulting in reduced fatal pulmonary embolism (25% of wild-type). Platelet aggregation and clot retraction after thrombin treatment is impaired. Platelet signaling and secretion is also defective. Activity induced seizures can occur in mutant mice over the age of seven months. This mutant mouse strain may be useful in studies of thrombosis and platelet aggregation. | ||
| 000002 | B6.C3-Pde6brd1 Hps4le/J | Repository- Live |
| 000305 | B6.Cg-Fbn1Tsk +/+ Pldnpa/J | Repository- Live |
| Mice homozygous for the pallid spontaneous mutation Pldnpa and nonagouti (a) have pink eyes and a light, yellow-brown coat. The Pldnpa/Pldnpa mice have a slightly lighter coat than strains that are homozygous for the pink-eyed dilution allele (Oca2p/Oca2p). Viability of homozygous mutant mice is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosi
..... For more information please see the full descriiption on the strain data sheet | ||
| 004201 | B6.Cg-Selplgtm1Fur/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted allele product (mRNA or protein) is detected by Northern blot or immunoassay. Mutant mice exhibit mild neutrophilia. Impaired early neutrophil migration in thioglycolate-induced peritonitis is followed by a delayed recovery to nearly normal levels. Although early trauma-induced leukocyte adhesion and migration is greatly reduced and in vivo leukocyte rolling (leukocyte-endothelial cell interaction) in postcapillary venules is severely decreased, cytokine-induced/E selectin-mediated leukocyte rolling is only slightly reduced in the mutant mice. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response. | ||
| 004669 | B6;129S2-Itgb3tm1Hyn/J | Repository- Live |
| Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed.
..... For more information please see the full descriiption on the strain data sheet | ||
| 003215 | B6Pin.C3-Ap3b1pe/J | Repository- Live |
| The homozygous pearl phenotype includes hypopigmentation of hair and eyes, prolonged bleeding times associated with platelet storage pool deficiency (SDP) and lysosomal accumulation of ceroid pigment. This combination of abnormalities is characteristic of a human hereditary disease, Hermansky-Pudlak syndrome. Pearl mice also exhibit reduced sensitivity in the dark-adapted state, altered somatostatin binding to the retina, and an increased rate of renal apoptosis, making them a potential model for human congenital stationary night blindness. | ||
| 007711 | C57BL/6J-Hps3coa-8J/J | Repository- Live |
| 003292 | 129S6/SvEvTac-Wastm1Sbs/J | Repository-Cryopreserved |
| WAS-deficient mice are viable and fertile. Mutant mice show normal lymphocyte development, serum immunoglobulin (Ig) levels and antibody responses. However, peripheral blood lymphocyte counts and platelet numbers are reduced in these mice. Development of chronic colitis is also observed. In vitro, WAS-deficient T cells show markedly impaired proliferative responses to anti-CD3e mediated stimulation. The Was gene is X-linked, so hemizygous males are WAS deficient. | ||
| 002472 | B10.A/SgSnJ-Hps3coa-5J/J | Repository-Cryopreserved |
| 000477 | B10.PA-Pldnpa H3e at/SnJ | Repository-Cryopreserved |
| This minor histocompatibility 3 (H3e) congenic strain is also carrying the closely linked pallid mutation (Pldnpa) as well as the black and tan allele of nonagouti also residing on Chromosome 2. Histocompatibility 3 is one of several loci isolated and identified by Dr. George Snell and co-workers. Histocompatibility gene differences were identified by generating congenic resistant strains and testing for resistance to transplantable tumors. Homozygous pallid mice have pink eyes, a diluted coat color and their viability is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manga
..... For more information please see the full descriiption on the strain data sheet | ||
| 000577 | B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J | Repository-Cryopreserved |
| 006184 | B6.129P2-Tbxas1tm1Swl/J | Repository-Cryopreserved |
| Homozygotes are viable and fertile with no gross physical or behavioral abnormalities. Northern blot show absence of a full length transcript in homozygous spleen and thymus. Homozygous mice exhibit prolonged bleeding time, defective platelet aggregation, and are protected from arachidonic acid induced-shock. These mice may be useful in studies of vascular biology, including hemostasis and thrombosis, as well as human TXAS-deficiency. | ||
| 004042 | B6.129S2-Alox12tm1Fun/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals. | ||
| 002862 | B6.129S4-F2rtm1Ajc/J | Repository-Cryopreserved |
| About half of the homozygous mice die at around embryonic day 9-10. The surviving homozygotes are fertile. Platelets from surviving homozygotes respond to thrombin while fibroblasts from the same mice are unable to respond to thrombin. | ||
| 002767 | B6.129S4-Nfe2tm1Sho/J | Repository-Cryopreserved |
| 90% of the homozygotes die within the first week of life. They display profound thrombocytopenia (no detectable circulating blood platelets) and megakaryocytes that show a maturation arrest characterized by failure to organize demarcatoin membranes and delimit platelet territories. Those that survive are anemic and display additional sporadic mortality of 10-20%. Male homozygotes are fertile. | ||
| 004202 | B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J | Repository-Cryopreserved |
| 000102 | B6.C3-Ap3b1pe/J | Repository-Cryopreserved |
| 000050 | B6.C3Fe-H51 Hps1ep /ByJ | Repository-Cryopreserved |
| 000525 | B6.C3Fe-Hps1ep/J | Repository-Cryopreserved |
| 000103 | B6.Cg-Hps6ru/J | Repository-Cryopreserved |
| 000204 | B6.Cg-Lystbg/J | Repository-Cryopreserved |
| Mice homozygous for the beige spontaneous mutation (Lystbg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l
..... For more information please see the full descriiption on the strain data sheet | ||
| 000024 | B6.Cg-Pldnpa/J | Repository-Cryopreserved |
| Mice homozygous for the pallid spontaneous mutation pa and nonagouti (a) are pink-eyed and have a light, yellow-brown coat. The coat is a little lighter than that of pink-eyed dilution homozygotes (p/p). Viability of homozygote mutant mice is slightly reduced. Some homoygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosidase, and a-mannosidase, accompanied by lowered enzyme excretion in the urine. Pallid mice have a deficiency in serum a1-antitrypsi
..... For more information please see the full descriiption on the strain data sheet | ||
| 000541 | B6.D2-Hps5ru2-hz/J | Repository-Cryopreserved |
| 004670 | B6;129S6-Abcg5/Abcg8tm1Hobb/J | Repository-Cryopreserved |
| Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in liver or jejunum. A 2 to 3 fold increase in fractional absorption of dietary plant sterols results in plasma sitosterol levels that are elevated 30 fold compared to wildtype levels. Biliary cholesterol levels are low, as are plasma and liver cholesterol levels. Plasma and liver cholesterol levels increase rapidly (2.4 and 18 fold, respectively) following cholesterol feeding. This mutant mouse strain represents a model that may be useful in studies related to sitosterolemia and cholesterol homeostasis. | ||
| 006182 | B6;129S6-Ptgs1tm1Fun/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Reduced gene product (protein) levels, 10% of wildtype levels, are detected by Western blot analysis of nonstimulated peritoneal macrophages. RT-PCR analysis of stomach and kidney tissue reveals that gene product (mRNA) levels are reduced by 70-73%. This allele is a hypomorph. Mutant mice have a reduced response to arachidonic acid and capsaicin evoked ear inflammation and to carrageenan induced paw edema. Platelet aggregation is impaired as indicated by resistance to arachidonic acid induced thrombosis in vivo, and failure to aggregate in response to arachidonic acid in vitro. Mutant mice exhibit lengthened bleeding time. This mutant mouse strain may be useful in studies related to inflammatory immune response and thrombosis. | ||
| 001025 | B6;B10-Hps3coa/J | Repository-Cryopreserved |
| 003542 | B6;SJL-Tg(FCGR2A)11Mkz/J | Repository-Cryopreserved |
| Studies of the immune destruction of blood cells, such as platelets in immune thrombocytopenia, serve as a model for exploring the pathophysiology of these disorders. In general, mice lack the genetic equivalent of human FCGR2A, which is the FC receptor for IgG. This strain expresses human FCGR2A on mouse platelets and macrophages at levels equivalent to that observed in human cells. Antibody-mediated thrombocytopenia is significantly more severe than that observed in wild type mice. There is no phenotype in the absence of anti-platelet antibodies. | ||
| 000604 | B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J | Repository-Cryopreserved |
| 000278 | B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J | Repository-Cryopreserved |
| 000232 | C3Fe.C3-Ap3b1pe/J | Repository-Cryopreserved |
| The homozygous pearl phenotype includes hypopigmentation of hair and eyes, prolonged bleeding times associated with platelet storage pool deficiency (SDP) and lysosomal accumulation of ceroid pigment. This combination of abnormalities is characteristic of a human hereditary disease, Hermansky-Pudlak syndrome. Pearl mice also exhibit reduced sensitivity in the dark-adapted state, altered somatostatin binding to the retina, and an increased rate of renal apoptosis, making them a potential model for human congenital stationary night blindness. | ||
| 003161 | C3H/HeJ-Hps3coa-6J/J | Repository-Cryopreserved |
| 000509 | C3H/HeJ-Lystbg-2J/J | Repository-Cryopreserved |
| Mice homozygous for the beige 2J spontaneous mutation (Lystbg-2J) display characteristics very similar to the original beige mutation (Lystbg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a
..... For more information please see the full descriiption on the strain data sheet | ||
| 000120 | C3H/HeSn-Rab27aash/J | Repository-Cryopreserved |
| Ashen mice have a lightened coat color that is gray on a non-agouti background similar to that of dilute (Myo5ad) or leaden (ln) mutants. Lane and Womack reported that on an agouti background the yellow pigment is more dilute in ashen mice resulting in a grayer agouti than that found in dilute or leaden mice, but Wu et al. subsequently reported that dilute and ashen mice have identical degrees of coat color dilution. This pigment dilution results from defective trafficking of melanosomes that are normally found throughout the dendrites of melanocytes. Similar to that seen in leaden mutants, ashen melanosomes are clumped around the nucleus and sparse in the dendrites where normally they are released. Melanosome trafficking from the melanocyte cell body to the ends of the dendrites results from a microtubule-based bidirectional transport. MYO5A is essential for retaining the melanosomes in the ends of the dendrites and preventing their retrograde transport back t
..... For more information please see the full descriiption on the strain data sheet | ||
| 000542 | C57BL/6J-Hps5ru2-J/J | Repository-Cryopreserved |
| 000110 | C57BL/6J-Rabggtagm/J | Repository-Cryopreserved |
| Mice homozygous for the Rabggtagm allele are grayish-black on a non-agouti background due to pigment dilution. Eye color is not affected. Homozygotes have reduced viability and do not breed well. These mutants have a prolonged bleeding time. Although gunmetal mice have an increased number of megakariocytes, they have about half the number platelets found in wildtype siblings. This decrease in platelet number results from a slower rate of platelet synthesis. These platelets are heterogeneous in size and are larger than normal, but have fewer dense granules per platelet and approximately half of the normal level of serotonin. The prolonged bleeding time and decreased platelet count and volume can be transferred to wildtype mice through bone marrow transplantion. Likewise bone marrow transplants from wildtype mice reversed the platelet deficiency in gunmetal recipients. Western blots of platelet extracts showed a decrease in fibrinogen, von Willebrand factor, and platel
..... For more information please see the full descriiption on the strain data sheet | ||
| 005124 | C57BL/6J-hlb219/J | Repository-Cryopreserved |
| For information on hlb219 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site. | ||
| 005343 | C57BL/6J-hlb381/J | Repository-Cryopreserved |
| For information on hlb381 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site. | ||
| 002531 | DBA/1LacJ-Ap3b1pe-7J/J | Repository-Cryopreserved |
| 002510 | DBA/2J-Ap3b1pe-8J/J | Repository-Cryopreserved |
| Appearance: Ap3b1pe-8J/Ap3b1pe-8J, lighter brown than normal DBA/2J mice. | ||
| 001594 | DBA/2J-Dtnbp1sdy/J | Repository-Cryopreserved |
| The autosomal recessive mutation sandy (sdy) takes its name from the lightened coat color first identified on the DBA/2J background. As early as 7-8 days of age the pinnae, feet, tail and fur are lighter in color than those of wildtype littermates and the lack of eye pigment is a defining trait at birth. The eye color does not darken with age unlike muted (mu) homozygotes. On the agouti C3H background, sandy homozygotes look like muted homozygotes, but on the non-agouti C57BL/6J or DBA/2J backgrounds, sandy homozygotes look like pallid (Pldnpa) homozygotes. The reduced pigmentation is linked to a storage pool deficiency. Sandy homozygotes have a prolonged bleeding time, in excess of 15 minutes, yet have normal platelet counts and normal sized platelets. Electron microscopy detects very few, if any, dense granules present in individual platelets of sandy homozygotes. Those that are detected are of normal size. Platelet serotonin levels are 7% that
..... For more information please see the full descriiption on the strain data sheet | ||
| 002712 | FVB/N-Tg(PF4MER)6Kra/J | Repository-Cryopreserved |
| Mice homozygous for this transgene are viable and fertile. Expression of the transgene is exclusively in platelets and megakaryocytes in female carrier mice or in male carrier mice given injections of estrogen. Megakaryopoiesis is increased and they exhibit essential thrombocythemia. This strains serves as a model for a myeloproliferative disorder resembling essential thrombocythemia. Also known as PF4MER. | ||
| 005941 | FVB/N-Tg(tetO-Aurkb,lacZ)41Kra/J | Repository-Cryopreserved |
| Hemizygous and homozygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is directed by a tetracycline-responsive regulatory element (TRE; tetO). When transgenic mice are bred with another transgenic strain expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, both aurora kinase B (Aurkb) and lacZ cistrons are inducibly expressed in the appropriate tissue in the bitransgenic offspring. This mouse was originally designed to be bred with Tg(Pf4-tTA)42Kra transgenic mice, which express tTA from a megakaryocyte-specific promoter. Megakaryocytes and platelet cells derived from the bitransgenic offspring show inducible and reversible beta-galactosidase expression. Further, megakaryocytes inducibly express Aurkb mRNA (but not protein) with a modest effect on megakaryocyte ploidy and no effect on platelet quant
..... | ||
| 000494 | J.Cg-Oca2+ Tyr+ Lystbg/J | Repository-Cryopreserved |
| Mice homozygous for the beige spontaneous mutation (Lystbg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l
..... For more information please see the full descriiption on the strain data sheet | ||
| 000259 | JE/LeJ | Repository-Cryopreserved |
| Mice homozygous for the jerker spontaneous mutation (Espnje) show behavior typical of the circling mutants - head-tossing, circling, and hyperactivity. Homozygous mutant mice are deaf from birth and have no detectable stimulus-related cochlear potential at any stage. The abnormal behavior and deafness are associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus in homozygotes. The primary influence of the jerker gene appears to be on the apical hair cells, not development of neural structures. Heterozygous jerker mice undergo a similar type of degeneration, but the onset is delayed. Auditory brainstem response is totally absent in homozygotes while heterozygous mice undergo a progressive impairment with age. JE/Le mice are also homozygous for the nonagouti (a), flexed tail (f), and ruby-eye (Hps6ru) mutations. | ||
| 000269 | SB/LeJ | Repository-Cryopreserved |
| The SB/Le inbred strain is homozygous for both the satin (Foxq1sa) and beige (Lystbg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo
..... For more information please see the full descriiption on the strain data sheet | ||
| 004655 | STOCK Gata1tm2Sho/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Reduced levels of gene product (mRNA) is detected by RT-PCR analysis. Mutant mice are thrombocytopenic and anemic at birth. Adult mutant mice have enlarged spleens and exhibit thrombocytopenia due to arrested megakaryocyte maturation which results in increased megakaryocytes in spleen and bone marrow. Platelet number in adult mutant mice is only 10% of wildtype. Erythroblast and mast cell differentiation is defective as indicated by increased apoptotic rates and accumulation of progenitors. Mutant mice display an enhanced response and recovery to experimentally induced acute and chronic erythropoiesis stimulation. At 15 months of age, homozygous female and heterozygous male mutant mice begin to develop idiopathic myelofibrosis-like symptoms including: anemia, tear-drop poikilocytes, progenitor cells in the blood, collagen fibers and o
..... For more information please see the full descriiption on the strain data sheet | ||
| 000279 | STOCK gr +/+ Ap3d1mh/J | Repository-Cryopreserved |
| Mice homozygous for the mocha spontaneous mutation (Ap3d1mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1mh allele have si
..... For more information please see the full descriiption on the strain data sheet | ||
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IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 003599 | B10.RIII H2r H2-T18b/(71NS)Sn-Ap3b1pe-11J/J | Research Strain |
| 006930 | B6.C3Fe-Hps1ep/JLlp | Research Strain |
| 006929 | B6.Cg-Hps6ru/JLlp | Research Strain |
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