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bone morphogenic protein 8b human  (Millipore)

 
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    Millipore bone morphogenic protein 8b human
    A. Representative whole cell current clamps traces from a glucose inhibited (GI) neuron in the ventrolateral ventromedial hypothalamus (vlVMH) in response to a glucose decrease from 2.5 to 0.1 mM glucose in the presence and absence of 1 nM bone morphogenetic protein (BMP) 8B. Top trace: This neuron depolarized and increased resistance in 0.1 mM glucose but returned to baseline before glucose was returned to 2.5 mM indicating that it belongs to the subcategory of adapting (Ad) GI neurons. Bottom trace: This depolarization and increased resistance was blocked in the presence of <t>BMP8B.</t> B. Representative voltage responses to a constant -20 pA hyperpolarizing current pulse in 2.5- and 0.1-mM glucose in the absence (top) and presence (bottom) of BMP8B. In the absence of BMP8B the voltage response increased in 0.1 mM glucose; however, BMP8B blocked this response. C. Bar graph of the percentage change in resistance as glucose was lowered from 2.5 to 0.1 mM glucose in the absence (con) and presence (BMP) of BMP8B. BMP8B significantly decreased the percentage change in resistance. Paired t-test. *p = 0.01. White square: AdGI neurons; black dot: sustained (s) GI neurons. D. Bar graph of the percentage of nNOS expressing cells that also express the BMP receptor BMPR1a in males and females. E. Immunohistochemical images of the VMH from males (left) and females (right) showing colocalization of neuronal nitric oxide synthase (nNOS, green) and BMPR1a (red). Dapi nuclear stain in blue. White arrows indicate cells expressing both nNOS and BMPR1a. F. Hypothetical model for the effect of BMP8B on VMH GI neurons. Glucose inhibits VMH nNOS-GI neurons by inhibiting AMPK. BMP8B also exerts it's metabolic effects by inhibiting VMH AMPK. Thus, BMP8B may regulate blood glucose in females due to increased expression of BMPR1a on nNOS expressing VMH GI neurons compared to males. * p<0.01, independent students t-test.
    Bone Morphogenic Protein 8b Human, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bone morphogenic protein 8b human/product/Millipore
    Average 90 stars, based on 1 article reviews
    bone morphogenic protein 8b human - by Bioz Stars, 2026-03
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    1) Product Images from "Bone morphogenetic protein 8B (BMP8B) increases the glucose sensitivity of ventromedial hypothalamus (VMH) glucose-inhibited (GI) neurons in female mice."

    Article Title: Bone morphogenetic protein 8B (BMP8B) increases the glucose sensitivity of ventromedial hypothalamus (VMH) glucose-inhibited (GI) neurons in female mice.

    Journal: microPublication Biology

    doi: 10.17912/micropub.biology.001496

    A. Representative whole cell current clamps traces from a glucose inhibited (GI) neuron in the ventrolateral ventromedial hypothalamus (vlVMH) in response to a glucose decrease from 2.5 to 0.1 mM glucose in the presence and absence of 1 nM bone morphogenetic protein (BMP) 8B. Top trace: This neuron depolarized and increased resistance in 0.1 mM glucose but returned to baseline before glucose was returned to 2.5 mM indicating that it belongs to the subcategory of adapting (Ad) GI neurons. Bottom trace: This depolarization and increased resistance was blocked in the presence of BMP8B. B. Representative voltage responses to a constant -20 pA hyperpolarizing current pulse in 2.5- and 0.1-mM glucose in the absence (top) and presence (bottom) of BMP8B. In the absence of BMP8B the voltage response increased in 0.1 mM glucose; however, BMP8B blocked this response. C. Bar graph of the percentage change in resistance as glucose was lowered from 2.5 to 0.1 mM glucose in the absence (con) and presence (BMP) of BMP8B. BMP8B significantly decreased the percentage change in resistance. Paired t-test. *p = 0.01. White square: AdGI neurons; black dot: sustained (s) GI neurons. D. Bar graph of the percentage of nNOS expressing cells that also express the BMP receptor BMPR1a in males and females. E. Immunohistochemical images of the VMH from males (left) and females (right) showing colocalization of neuronal nitric oxide synthase (nNOS, green) and BMPR1a (red). Dapi nuclear stain in blue. White arrows indicate cells expressing both nNOS and BMPR1a. F. Hypothetical model for the effect of BMP8B on VMH GI neurons. Glucose inhibits VMH nNOS-GI neurons by inhibiting AMPK. BMP8B also exerts it's metabolic effects by inhibiting VMH AMPK. Thus, BMP8B may regulate blood glucose in females due to increased expression of BMPR1a on nNOS expressing VMH GI neurons compared to males. * p<0.01, independent students t-test.
    Figure Legend Snippet: A. Representative whole cell current clamps traces from a glucose inhibited (GI) neuron in the ventrolateral ventromedial hypothalamus (vlVMH) in response to a glucose decrease from 2.5 to 0.1 mM glucose in the presence and absence of 1 nM bone morphogenetic protein (BMP) 8B. Top trace: This neuron depolarized and increased resistance in 0.1 mM glucose but returned to baseline before glucose was returned to 2.5 mM indicating that it belongs to the subcategory of adapting (Ad) GI neurons. Bottom trace: This depolarization and increased resistance was blocked in the presence of BMP8B. B. Representative voltage responses to a constant -20 pA hyperpolarizing current pulse in 2.5- and 0.1-mM glucose in the absence (top) and presence (bottom) of BMP8B. In the absence of BMP8B the voltage response increased in 0.1 mM glucose; however, BMP8B blocked this response. C. Bar graph of the percentage change in resistance as glucose was lowered from 2.5 to 0.1 mM glucose in the absence (con) and presence (BMP) of BMP8B. BMP8B significantly decreased the percentage change in resistance. Paired t-test. *p = 0.01. White square: AdGI neurons; black dot: sustained (s) GI neurons. D. Bar graph of the percentage of nNOS expressing cells that also express the BMP receptor BMPR1a in males and females. E. Immunohistochemical images of the VMH from males (left) and females (right) showing colocalization of neuronal nitric oxide synthase (nNOS, green) and BMPR1a (red). Dapi nuclear stain in blue. White arrows indicate cells expressing both nNOS and BMPR1a. F. Hypothetical model for the effect of BMP8B on VMH GI neurons. Glucose inhibits VMH nNOS-GI neurons by inhibiting AMPK. BMP8B also exerts it's metabolic effects by inhibiting VMH AMPK. Thus, BMP8B may regulate blood glucose in females due to increased expression of BMPR1a on nNOS expressing VMH GI neurons compared to males. * p<0.01, independent students t-test.

    Techniques Used: Expressing, Immunohistochemical staining, Staining



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    bone morphogenic protein 8b human  (Millipore)
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    Millipore bone morphogenic protein 8b human
    A. Representative whole cell current clamps traces from a glucose inhibited (GI) neuron in the ventrolateral ventromedial hypothalamus (vlVMH) in response to a glucose decrease from 2.5 to 0.1 mM glucose in the presence and absence of 1 nM bone morphogenetic protein (BMP) 8B. Top trace: This neuron depolarized and increased resistance in 0.1 mM glucose but returned to baseline before glucose was returned to 2.5 mM indicating that it belongs to the subcategory of adapting (Ad) GI neurons. Bottom trace: This depolarization and increased resistance was blocked in the presence of <t>BMP8B.</t> B. Representative voltage responses to a constant -20 pA hyperpolarizing current pulse in 2.5- and 0.1-mM glucose in the absence (top) and presence (bottom) of BMP8B. In the absence of BMP8B the voltage response increased in 0.1 mM glucose; however, BMP8B blocked this response. C. Bar graph of the percentage change in resistance as glucose was lowered from 2.5 to 0.1 mM glucose in the absence (con) and presence (BMP) of BMP8B. BMP8B significantly decreased the percentage change in resistance. Paired t-test. *p = 0.01. White square: AdGI neurons; black dot: sustained (s) GI neurons. D. Bar graph of the percentage of nNOS expressing cells that also express the BMP receptor BMPR1a in males and females. E. Immunohistochemical images of the VMH from males (left) and females (right) showing colocalization of neuronal nitric oxide synthase (nNOS, green) and BMPR1a (red). Dapi nuclear stain in blue. White arrows indicate cells expressing both nNOS and BMPR1a. F. Hypothetical model for the effect of BMP8B on VMH GI neurons. Glucose inhibits VMH nNOS-GI neurons by inhibiting AMPK. BMP8B also exerts it's metabolic effects by inhibiting VMH AMPK. Thus, BMP8B may regulate blood glucose in females due to increased expression of BMPR1a on nNOS expressing VMH GI neurons compared to males. * p<0.01, independent students t-test.
    Bone Morphogenic Protein 8b Human, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bone morphogenic protein 8b human/product/Millipore
    Average 90 stars, based on 1 article reviews
    bone morphogenic protein 8b human - by Bioz Stars, 2026-03
    90/100 stars
    		  Buy from Supplier

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    A. Representative whole cell current clamps traces from a glucose inhibited (GI) neuron in the ventrolateral ventromedial hypothalamus (vlVMH) in response to a glucose decrease from 2.5 to 0.1 mM glucose in the presence and absence of 1 nM bone morphogenetic protein (BMP) 8B. Top trace: This neuron depolarized and increased resistance in 0.1 mM glucose but returned to baseline before glucose was returned to 2.5 mM indicating that it belongs to the subcategory of adapting (Ad) GI neurons. Bottom trace: This depolarization and increased resistance was blocked in the presence of BMP8B. B. Representative voltage responses to a constant -20 pA hyperpolarizing current pulse in 2.5- and 0.1-mM glucose in the absence (top) and presence (bottom) of BMP8B. In the absence of BMP8B the voltage response increased in 0.1 mM glucose; however, BMP8B blocked this response. C. Bar graph of the percentage change in resistance as glucose was lowered from 2.5 to 0.1 mM glucose in the absence (con) and presence (BMP) of BMP8B. BMP8B significantly decreased the percentage change in resistance. Paired t-test. *p = 0.01. White square: AdGI neurons; black dot: sustained (s) GI neurons. D. Bar graph of the percentage of nNOS expressing cells that also express the BMP receptor BMPR1a in males and females. E. Immunohistochemical images of the VMH from males (left) and females (right) showing colocalization of neuronal nitric oxide synthase (nNOS, green) and BMPR1a (red). Dapi nuclear stain in blue. White arrows indicate cells expressing both nNOS and BMPR1a. F. Hypothetical model for the effect of BMP8B on VMH GI neurons. Glucose inhibits VMH nNOS-GI neurons by inhibiting AMPK. BMP8B also exerts it's metabolic effects by inhibiting VMH AMPK. Thus, BMP8B may regulate blood glucose in females due to increased expression of BMPR1a on nNOS expressing VMH GI neurons compared to males. * p<0.01, independent students t-test.

    Journal: microPublication Biology

    Article Title: Bone morphogenetic protein 8B (BMP8B) increases the glucose sensitivity of ventromedial hypothalamus (VMH) glucose-inhibited (GI) neurons in female mice.

    doi: 10.17912/micropub.biology.001496

    Figure Lengend Snippet: A. Representative whole cell current clamps traces from a glucose inhibited (GI) neuron in the ventrolateral ventromedial hypothalamus (vlVMH) in response to a glucose decrease from 2.5 to 0.1 mM glucose in the presence and absence of 1 nM bone morphogenetic protein (BMP) 8B. Top trace: This neuron depolarized and increased resistance in 0.1 mM glucose but returned to baseline before glucose was returned to 2.5 mM indicating that it belongs to the subcategory of adapting (Ad) GI neurons. Bottom trace: This depolarization and increased resistance was blocked in the presence of BMP8B. B. Representative voltage responses to a constant -20 pA hyperpolarizing current pulse in 2.5- and 0.1-mM glucose in the absence (top) and presence (bottom) of BMP8B. In the absence of BMP8B the voltage response increased in 0.1 mM glucose; however, BMP8B blocked this response. C. Bar graph of the percentage change in resistance as glucose was lowered from 2.5 to 0.1 mM glucose in the absence (con) and presence (BMP) of BMP8B. BMP8B significantly decreased the percentage change in resistance. Paired t-test. *p = 0.01. White square: AdGI neurons; black dot: sustained (s) GI neurons. D. Bar graph of the percentage of nNOS expressing cells that also express the BMP receptor BMPR1a in males and females. E. Immunohistochemical images of the VMH from males (left) and females (right) showing colocalization of neuronal nitric oxide synthase (nNOS, green) and BMPR1a (red). Dapi nuclear stain in blue. White arrows indicate cells expressing both nNOS and BMPR1a. F. Hypothetical model for the effect of BMP8B on VMH GI neurons. Glucose inhibits VMH nNOS-GI neurons by inhibiting AMPK. BMP8B also exerts it's metabolic effects by inhibiting VMH AMPK. Thus, BMP8B may regulate blood glucose in females due to increased expression of BMPR1a on nNOS expressing VMH GI neurons compared to males. * p<0.01, independent students t-test.

    Article Snippet: Materials: Bone Morphogenic Protein 8B (BMP8B) human (Millipore Sigma, SRP 6322, Burlington, MA), Antibodies: primary rabbit anti-NOS1 (1:200, Cell Signaling Technology C7D7,Danvers, MA), secondary Alexa FluorTM 488 (1:500, Donkey anti-Rabbit; A21206, Invitrogen, Waltham, MA); primary mouse Anti-BMPR1A (1:250, Santa Cruz Biotechnology, sc293175, Dallas, TX), secondary Alexa FluorTM 594 (1:500, Donkey anti -Mouse; A21203, Invitrogen, Waltham, MA) Cell Counting: Images were obtained using the Nikon A1R Confocal Laser Microscope System.

    Techniques: Expressing, Immunohistochemical staining, Staining