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Eif2ak3tm1.2drc

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The Eif2ak3tm1.2Drc is a laboratory equipment product produced by Jackson ImmunoResearch. It serves a core function related to research applications, but a detailed description cannot be provided while maintaining an unbiased and factual approach without extrapolation.

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Lab products found in correlation

Mmtv cre, by Jackson ImmunoResearch (2 mentions) Tg mmtv cre 4mam, by Jackson ImmunoResearch (2 mentions)

2 protocols using eif2ak3tm1.2drc

1

Generation of Fatty Acid-Deficient Mammary Milk

Check if the same lab product or an alternative is used in the 5 most similar protocols
The Protein Kinase R (PKR)-like endoplasmic reticulum kinase (PERK) or
Eukaryotic translation initiation factor 2 alpha-subunit kinase 3 (Eif2ak3)
plays a significant role in the unfolded protein response55 (link),56 (link). PERK is required for proper development and maturation of
mammary epithelial cells. Deletion of PERK in mammary glands inhibits key
lipogenic enzymes involved in lipid production and storage (Fatty acid synthase,
ATP citrate lyase and stearyl-CoA desaturase-1) decreasing the lipid content in
milk45 (link). To generate
mice which produce milk deficient in fatty acids, PERKloxP mice with
loxP sites which flank exons 3–557 (link) were mated with Mouse mammary tumor virus (MMTV)-Cre
transgenic mice46 (link). MMTV-cre
transgenic mouse lines express Cre recombinase predominantly in secretory cell
types in the mammary epithelium46 (link). Female mice homozygous for PERKloxP and
MMTV-cre produce mammary glands in which the milk is deficient in fatty
acids45 (link). Here, only
male mice were used in our studies to avoid variations between groups. The
PERKloxP and MMTV-cre mice were obtained from Jackson Laboratory
(Eif2ak3tm1.2Drc stock number 023066); and Tg(MMTV-cre)4Mam -
stock number 003553), respectively.
Cardoso A.C., Lam N.T., Savla J.J., Nakada Y., Pereira A.H., Elnwasany A., Menendez-Montes I., Ensley E.L., Petric U.B., Sharma G., Sherry A.D., Malloy C.R., Khemtong C., Kinter M.T., Tan W.L., Anene-Nzelu C.G., Foo R.S., Nguyen N.U., Li S., Ahmed M.S., Elhelaly W.M., Abdisalaam S., Asaithamby A., Xing C., Kanchwala M., Vale G., Eckert K.M., Mitsche M.A., McDonald J.G., Hill J.A., Huang L., Shaul P.W., Szweda L.I, & Sadek H.A. (2020). Mitochondrial Substrate Utilization Regulates Cardiomyocyte Cell Cycle Progression. Nature metabolism, 2(2), 167-178.
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2

Generation of Fatty Acid-Deficient Mammary Milk

Check if the same lab product or an alternative is used in the 5 most similar protocols
The Protein Kinase R (PKR)-like endoplasmic reticulum kinase (PERK) or
Eukaryotic translation initiation factor 2 alpha-subunit kinase 3 (Eif2ak3)
plays a significant role in the unfolded protein response55 (link),56 (link). PERK is required for proper development and maturation of
mammary epithelial cells. Deletion of PERK in mammary glands inhibits key
lipogenic enzymes involved in lipid production and storage (Fatty acid synthase,
ATP citrate lyase and stearyl-CoA desaturase-1) decreasing the lipid content in
milk45 (link). To generate
mice which produce milk deficient in fatty acids, PERKloxP mice with
loxP sites which flank exons 3–557 (link) were mated with Mouse mammary tumor virus (MMTV)-Cre
transgenic mice46 (link). MMTV-cre
transgenic mouse lines express Cre recombinase predominantly in secretory cell
types in the mammary epithelium46 (link). Female mice homozygous for PERKloxP and
MMTV-cre produce mammary glands in which the milk is deficient in fatty
acids45 (link). Here, only
male mice were used in our studies to avoid variations between groups. The
PERKloxP and MMTV-cre mice were obtained from Jackson Laboratory
(Eif2ak3tm1.2Drc stock number 023066); and Tg(MMTV-cre)4Mam -
stock number 003553), respectively.
Cardoso A.C., Lam N.T., Savla J.J., Nakada Y., Pereira A.H., Elnwasany A., Menendez-Montes I., Ensley E.L., Petric U.B., Sharma G., Sherry A.D., Malloy C.R., Khemtong C., Kinter M.T., Tan W.L., Anene-Nzelu C.G., Foo R.S., Nguyen N.U., Li S., Ahmed M.S., Elhelaly W.M., Abdisalaam S., Asaithamby A., Xing C., Kanchwala M., Vale G., Eckert K.M., Mitsche M.A., McDonald J.G., Hill J.A., Huang L., Shaul P.W., Szweda L.I, & Sadek H.A. (2020). Mitochondrial Substrate Utilization Regulates Cardiomyocyte Cell Cycle Progression. Nature metabolism, 2(2), 167-178.
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