Examples of referencing styles
Reference style ( MLA 8th edition )
Hemoglobinopathies are a group of inherited hemoglobin disorders caused by structural or
molecular abnormalities in hemoglobin (Weatherall and Clegg). Sickle cell disease (SCD) and
β-thalassemia are the most common hemoglobinopathies worldwide, which pose a serious
public health issue (Rees et al.). Sickle hemoglobin (HbS, α2βS2) produced due to single point
mutation in the β-globin gene (Rees et al.). Deoxygenation of HbS leads to polymerization,
which causes erythrocyte deformation and blood hemolysis, resulting in severe clinical
complications (Platt). Hemoglobin A2 (HbA2, α2δ2) and HbF (α2γ2) are both found in adult
blood at low levels (Steinberg and Adams) (Rochette et al.). Furthermore, the absence of a
KLF1-binding site within -globin results in low HbA2 expression(Tang et al.). Previous study
had shown that Interaction between δ globin and KLF1-GATA1 fusion protein could increase
δ globin expression (Zhu et al.). In recent study, they demonstrate the effect of the KLF1-
GATA1 fusion protein on HbA2 expression and correction of the SCD phenotype in vivo and
in vitro (Zhu, Li, et al.). They found a significant increase in δ globin expression and reduction
of hypoxia-related sickling in SCD human and mouse erythrocytes due to forced expression of
medium and long forms of the KLF1-GATA1 fusion protein (Zhu, Li, et al.). Furthermore,
transduction by the KLF1-GATA1 fusion protein had no effect on human sickle CD34+
erythroid cells' differentiation and proliferation (Zhu, Li, et al.). Study result suggest that
KLF1-GATA1 fusion proteins could be useful as a genetic therapeutic tool for SCD and β-
thalassemia (Zhu, Li, et al.).
References
1- Weatherall, D. J., and J. B. Clegg. “Inherited Haemoglobin Disorders: An Increasing
Global Health Problem.” Bulletin of the World Health Organization, vol. 79, no. 8,
2001, pp. 704–712, https://pubmed.ncbi.nlm.nih.gov/11545326/.
2- Rees, David C., et al. “Sickle-Cell Disease.” Lancet, vol. 376, no. 9757, 2010, pp.
2018–2031, doi:10.1016/S0140-6736(10)61029-X.
3- Platt, Orah S. “Hydroxyurea for the Treatment of Sickle Cell Anemia.” The New
England Journal of Medicine, vol. 358, no. 13, 2008, pp. 1362–1369,
doi:10.1056/NEJMct0708272.
4- Steinberg, M. H., and J. G. Adams 3rd. “Hemoglobin A2: Origin, Evolution, and
Aftermath.” Blood, vol. 78, no. 9, 1991, pp. 2165–2177,
https://pubmed.ncbi.nlm.nih.gov/1932737/.
5- Rochette, J., et al. “Fetal Hemoglobin Levels in Adults.” Blood Reviews, vol. 8, no. 4,
1994, pp. 213–224, doi:10.1016/0268-960x(94)90109-0.
6- Tang, D. C., et al. “Restoration of the CCAAT Box or Insertion of the CACCC Motif
Activates [Corrected] Delta-Globin Gene Expression.” Blood, vol. 90, no. 1, 1997, pp.
421–427, https://pubmed.ncbi.nlm.nih.gov/9207479/.
7- Zhu, Jianqiong, et al. “Recombinant Erythroid Kruppel-like Factor Fused to GATA1
up-Regulates Delta- and Gamma-Globin Expression in Erythroid Cells.” Blood, vol.
117, no. 11, 2011, pp. 3045–3052, doi:10.1182/blood-2010-07-294751.
8- Zhu, Jianqiong, Hongzhen Li, et al. “Kruppel-like Factor 1-GATA1 Fusion Protein
Improves the Sickle Cell Disease Phenotype in Mice Both in Vitro and in Vivo.” Blood,
vol. 140, no. 21, 2022, pp. 2276–2289, doi:10.1182/blood.2021014877.
, Reference style ( APA 7th edition )
Hemoglobinopathies are a group of inherited hemoglobin disorders caused by structural or
molecular abnormalities in hemoglobin (Weatherall & Clegg, 2001). Sickle cell disease (SCD)
and β-thalassemia are the most common hemoglobinopathies worldwide, which pose a serious
public health issue (Rees et al., 2010). Sickle hemoglobin (HbS, α2βS2) produced due to single
point mutation in the β-globin gene (Rees et al., 2010). Deoxygenation of HbS leads to
polymerization, which causes erythrocyte deformation and blood hemolysis, resulting in severe
clinical complications (Platt, 2008). Hemoglobin A2 (HbA2, α2δ2) and HbF (α2γ2) are both
found in adult blood at low levels (Steinberg & Adams, 1991) (Rochette et al., 1994).
Furthermore, the absence of a KLF1-binding site within -globin results in low HbA2 expression
(Tang et al., 1997). Previous study had shown that Interaction between δ globin and KLF1-
GATA1 fusion protein could increase δ globin expression (Zhu et al., 2011). In recent study,
they demonstrate the effect of the KLF1-GATA1 fusion protein on HbA2 expression and
correction of the SCD phenotype in vivo and in vitro (Zhu et al., 2022). They found a
significant increase in δ globin expression and reduction of hypoxia-related sickling in SCD
human and mouse erythrocytes due to forced expression of medium and long forms of the
KLF1-GATA1 fusion protein (Zhu et al., 2022). Furthermore, transduction by the KLF1-
GATA1 fusion protein had no effect on human sickle CD34+ erythroid cells' differentiation
and proliferation (Zhu et al., 2022). Study result suggest that KLF1-GATA1 fusion proteins
could be useful as a genetic therapeutic tool for SCD and β-thalassemia (Zhu et al., 2022).
References
1- Weatherall, D. J., & Clegg, J. B. (2001). Inherited haemoglobin disorders: an increasing
global health problem. Bulletin of the World Health Organization, 79(8), 704–712.
https://pubmed.ncbi.nlm.nih.gov/11545326/
2- Rees, D. C., Williams, T. N., & Gladwin, M. T. (2010). Sickle-cell
disease. Lancet, 376(9757), 2018–2031. https://doi.org/10.1016/S0140-
6736(10)61029-X
3- Platt, O. S. (2008). Hydroxyurea for the treatment of sickle cell anemia. The New
England Journal of Medicine, 358(13), 1362–1369.
https://doi.org/10.1056/NEJMct0708272
4- Steinberg, M. H., & Adams, J. G., 3rd. (1991). Hemoglobin A2: origin, evolution, and
aftermath. Blood, 78(9), 2165–2177. https://pubmed.ncbi.nlm.nih.gov/1932737/
5- Rochette, J., Craig, J. E., Thein, S. L., & Rochette, J. (1994). Fetal hemoglobin levels
in adults. Blood Reviews, 8(4), 213–224. https://doi.org/10.1016/0268-960x(94)90109-
0
6- Tang, D. C., Ebb, D., Hardison, R. C., & Rodgers, G. P. (1997). Restoration of the
CCAAT box or insertion of the CACCC motif activates [corrected] delta-globin gene
expression. Blood, 90(1), 421–427. https://pubmed.ncbi.nlm.nih.gov/9207479/
7- Zhu, J., Chin, K., Aerbajinai, W., Trainor, C., Gao, P., & Rodgers, G. P. (2011).
Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and
gamma-globin expression in erythroid cells. Blood, 117(11), 3045–3052.
https://doi.org/10.1182/blood-2010-07-294751
8- Zhu, J., Li, H., Aerbajinai, W., Kumkhaek, C., Pirooznia, M., Saxena, A., Dagur, P.,
Chin, K., & Rodgers, G. P. (2022). Kruppel-like factor 1-GATA1 fusion protein
improves the sickle cell disease phenotype in mice both in vitro and in
vivo. Blood, 140(21), 2276–2289. https://doi.org/10.1182/blood.2021014877
Reference style ( MLA 8th edition )
Hemoglobinopathies are a group of inherited hemoglobin disorders caused by structural or
molecular abnormalities in hemoglobin (Weatherall and Clegg). Sickle cell disease (SCD) and
β-thalassemia are the most common hemoglobinopathies worldwide, which pose a serious
public health issue (Rees et al.). Sickle hemoglobin (HbS, α2βS2) produced due to single point
mutation in the β-globin gene (Rees et al.). Deoxygenation of HbS leads to polymerization,
which causes erythrocyte deformation and blood hemolysis, resulting in severe clinical
complications (Platt). Hemoglobin A2 (HbA2, α2δ2) and HbF (α2γ2) are both found in adult
blood at low levels (Steinberg and Adams) (Rochette et al.). Furthermore, the absence of a
KLF1-binding site within -globin results in low HbA2 expression(Tang et al.). Previous study
had shown that Interaction between δ globin and KLF1-GATA1 fusion protein could increase
δ globin expression (Zhu et al.). In recent study, they demonstrate the effect of the KLF1-
GATA1 fusion protein on HbA2 expression and correction of the SCD phenotype in vivo and
in vitro (Zhu, Li, et al.). They found a significant increase in δ globin expression and reduction
of hypoxia-related sickling in SCD human and mouse erythrocytes due to forced expression of
medium and long forms of the KLF1-GATA1 fusion protein (Zhu, Li, et al.). Furthermore,
transduction by the KLF1-GATA1 fusion protein had no effect on human sickle CD34+
erythroid cells' differentiation and proliferation (Zhu, Li, et al.). Study result suggest that
KLF1-GATA1 fusion proteins could be useful as a genetic therapeutic tool for SCD and β-
thalassemia (Zhu, Li, et al.).
References
1- Weatherall, D. J., and J. B. Clegg. “Inherited Haemoglobin Disorders: An Increasing
Global Health Problem.” Bulletin of the World Health Organization, vol. 79, no. 8,
2001, pp. 704–712, https://pubmed.ncbi.nlm.nih.gov/11545326/.
2- Rees, David C., et al. “Sickle-Cell Disease.” Lancet, vol. 376, no. 9757, 2010, pp.
2018–2031, doi:10.1016/S0140-6736(10)61029-X.
3- Platt, Orah S. “Hydroxyurea for the Treatment of Sickle Cell Anemia.” The New
England Journal of Medicine, vol. 358, no. 13, 2008, pp. 1362–1369,
doi:10.1056/NEJMct0708272.
4- Steinberg, M. H., and J. G. Adams 3rd. “Hemoglobin A2: Origin, Evolution, and
Aftermath.” Blood, vol. 78, no. 9, 1991, pp. 2165–2177,
https://pubmed.ncbi.nlm.nih.gov/1932737/.
5- Rochette, J., et al. “Fetal Hemoglobin Levels in Adults.” Blood Reviews, vol. 8, no. 4,
1994, pp. 213–224, doi:10.1016/0268-960x(94)90109-0.
6- Tang, D. C., et al. “Restoration of the CCAAT Box or Insertion of the CACCC Motif
Activates [Corrected] Delta-Globin Gene Expression.” Blood, vol. 90, no. 1, 1997, pp.
421–427, https://pubmed.ncbi.nlm.nih.gov/9207479/.
7- Zhu, Jianqiong, et al. “Recombinant Erythroid Kruppel-like Factor Fused to GATA1
up-Regulates Delta- and Gamma-Globin Expression in Erythroid Cells.” Blood, vol.
117, no. 11, 2011, pp. 3045–3052, doi:10.1182/blood-2010-07-294751.
8- Zhu, Jianqiong, Hongzhen Li, et al. “Kruppel-like Factor 1-GATA1 Fusion Protein
Improves the Sickle Cell Disease Phenotype in Mice Both in Vitro and in Vivo.” Blood,
vol. 140, no. 21, 2022, pp. 2276–2289, doi:10.1182/blood.2021014877.
, Reference style ( APA 7th edition )
Hemoglobinopathies are a group of inherited hemoglobin disorders caused by structural or
molecular abnormalities in hemoglobin (Weatherall & Clegg, 2001). Sickle cell disease (SCD)
and β-thalassemia are the most common hemoglobinopathies worldwide, which pose a serious
public health issue (Rees et al., 2010). Sickle hemoglobin (HbS, α2βS2) produced due to single
point mutation in the β-globin gene (Rees et al., 2010). Deoxygenation of HbS leads to
polymerization, which causes erythrocyte deformation and blood hemolysis, resulting in severe
clinical complications (Platt, 2008). Hemoglobin A2 (HbA2, α2δ2) and HbF (α2γ2) are both
found in adult blood at low levels (Steinberg & Adams, 1991) (Rochette et al., 1994).
Furthermore, the absence of a KLF1-binding site within -globin results in low HbA2 expression
(Tang et al., 1997). Previous study had shown that Interaction between δ globin and KLF1-
GATA1 fusion protein could increase δ globin expression (Zhu et al., 2011). In recent study,
they demonstrate the effect of the KLF1-GATA1 fusion protein on HbA2 expression and
correction of the SCD phenotype in vivo and in vitro (Zhu et al., 2022). They found a
significant increase in δ globin expression and reduction of hypoxia-related sickling in SCD
human and mouse erythrocytes due to forced expression of medium and long forms of the
KLF1-GATA1 fusion protein (Zhu et al., 2022). Furthermore, transduction by the KLF1-
GATA1 fusion protein had no effect on human sickle CD34+ erythroid cells' differentiation
and proliferation (Zhu et al., 2022). Study result suggest that KLF1-GATA1 fusion proteins
could be useful as a genetic therapeutic tool for SCD and β-thalassemia (Zhu et al., 2022).
References
1- Weatherall, D. J., & Clegg, J. B. (2001). Inherited haemoglobin disorders: an increasing
global health problem. Bulletin of the World Health Organization, 79(8), 704–712.
https://pubmed.ncbi.nlm.nih.gov/11545326/
2- Rees, D. C., Williams, T. N., & Gladwin, M. T. (2010). Sickle-cell
disease. Lancet, 376(9757), 2018–2031. https://doi.org/10.1016/S0140-
6736(10)61029-X
3- Platt, O. S. (2008). Hydroxyurea for the treatment of sickle cell anemia. The New
England Journal of Medicine, 358(13), 1362–1369.
https://doi.org/10.1056/NEJMct0708272
4- Steinberg, M. H., & Adams, J. G., 3rd. (1991). Hemoglobin A2: origin, evolution, and
aftermath. Blood, 78(9), 2165–2177. https://pubmed.ncbi.nlm.nih.gov/1932737/
5- Rochette, J., Craig, J. E., Thein, S. L., & Rochette, J. (1994). Fetal hemoglobin levels
in adults. Blood Reviews, 8(4), 213–224. https://doi.org/10.1016/0268-960x(94)90109-
0
6- Tang, D. C., Ebb, D., Hardison, R. C., & Rodgers, G. P. (1997). Restoration of the
CCAAT box or insertion of the CACCC motif activates [corrected] delta-globin gene
expression. Blood, 90(1), 421–427. https://pubmed.ncbi.nlm.nih.gov/9207479/
7- Zhu, J., Chin, K., Aerbajinai, W., Trainor, C., Gao, P., & Rodgers, G. P. (2011).
Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and
gamma-globin expression in erythroid cells. Blood, 117(11), 3045–3052.
https://doi.org/10.1182/blood-2010-07-294751
8- Zhu, J., Li, H., Aerbajinai, W., Kumkhaek, C., Pirooznia, M., Saxena, A., Dagur, P.,
Chin, K., & Rodgers, G. P. (2022). Kruppel-like factor 1-GATA1 fusion protein
improves the sickle cell disease phenotype in mice both in vitro and in
vivo. Blood, 140(21), 2276–2289. https://doi.org/10.1182/blood.2021014877
