a, B, c (also carries black)
Albino
Genes:

Car-2^a, Ce-2^b, Es-1^b, Es-3^c, Es-10^b, Gpd-1^b, Gpi-1^a, Gus^b, Hbb^d, Idh-1^b, Lv^a, Mod-1^b, Mup-1^a, Pep-3^b, Pgm-1^a, Trf^b
Hc⁰, H-2D^k, H-2K^k, Lyb-2^c, Lyt-1^b, Lyt-2^a, Lyt-3^a, Thy-1^a, Tla^b.

• Leukemia incidence was significantly higher in females (92.6%) than males (79.7%) and the lifespan was shorter in females (38.5 weeks) than males (44.4 weeks). No mammary tumors were observed but foster nursing by strain 1194 indicated their susceptibility. (428)

• In comparison with other inbred strains, AKR is susceptible to Gross virus, relatively susceptible to Friend S and Friend B viruses, and resistant to Vaccinia virus. (370)
• Sensitive to Graffi leukemia agent. (189)

• Obstructive uropathy in 13% of males and 7% of females. (027)

• Expression of XenCSA is low on thymic and high on splenic lymphocytes. (488)
• Has the autosomal dominant gene which confers hybrid resistance bo BALB/c plasmacytoma MPC-11, and is resistant to tumor take. (768)
• Allergenicity of concanavalin A is low to intermediate in this strain. (468)
• Young (AKR x BALB/c)F₁ mice spleen cell cultures spontaneously develop cytotoxic t lymphocytes (CTL) in the absence of parental stimulation, lysing ARK, BALB/c, and F1 target cells, but not cells from unrelated strains. The target antigen for spontaneous CTL of young F₁ is indistinguishable from those of induced adult F₁. (326,327)
• Three independently segregating viral loci, all of which code for an ecotropic virus, are expressed early in life; site of proviral integration is strain specific. (318)
• MuLv gp 71 specific T cell blastogenesis in vitro is detectable throughout preleukemic phase or the first five months in contrast to non-viremic, non-leukemic strains and F₁ crosses where it is detected only during first two months. Persistent gp 71 blastogenic response segregates with viremia and leukemia. (395)
• AKR is one of few strains (7 out of 38 tested) that is Thy-1^a (thy 1.1+). (564, 576)
• Preleukemic AKR mice have lower levels of IgG₁ and IgA than C3H controls but equivalent IgM. Recriprocal bone marrow transplants indicate that the very low IgA is a result of a genetically determined prevention of IgA synthesis. (751)
• Alloimmunization of CBA induces a population of cells which when transplanted to AKR leukemic mice led to destruction of disseminated leukemia (AKR-L) cells. The transplanted cells did not cause augmentation of graft-vs-host disease seen when cells from unimmunized CBA donors were administered to lethally irradiated AKR hosts. (073)
• Not responsive to pertussis HSF. (778,500)
• High producers of interferon after Newcastle disease virus induction. (696)
• After treatment with BCG and grafting with spontaneous AKR leukemia cells, AKR mice either (1) develop leukemia (graft or spontaneous), (2) die in a wasting syndrome, or (3) are cured from leukemia without signs of wasting-like syndrome. Spleen cells from cured mice or mice with the wasting syndrome, but not from leukemic mice, inhibit cytotoxic activity of otherwise cytotoxic cells indicating suppressor activity in cured mice. (525)
• C5 deficiency attributed to failure in biosynthesis of proC5 single chain precursor. (526)

• Aryl hydrocarbon hydroxylase not induced by polycyclis aromatic hydrocarbons. The nonresponsive Ah^d allele is present. (737,664)

• Low resting steroid levels in plasma, peak only briefly after stress. (398)

• Benzo(a)phyrene administration at day 7 or 10 of gestation caused less in utero toxicity and teratogenicity in AKR than in C57BL/6 mice. Allelic differences at th Ah locus in the fetus were correlated with dysmorphogenesis. (664)
• AKR chromosomes contain genome of ecotropic MuLV at two loci, Akv-1 and Akv-2. (577)